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PMID	16505175 ( )
Title	Glycated proteins stimulate reactive oxygen species production in cardiac myocytes: involvement of Nox2 (gp91phox)-containing NADPH oxidase.
Abstract	BACKGROUND: Nonenzymatic glycation that results in the production of early-glycation Amadori-modified proteins and advanced-glycation end products may be important in the pathogenesis of diabetic complications. However, the effects of early-glycated proteins, such as glycated serum albumin (Gly-BSA), are poorly defined. In this study, we investigated the effects of Gly-BSA on reactive oxygen species (ROS) production by cardiomyocytes. METHODS AND RESULTS: Cultured neonatal rat cardiomyocytes were incubated with Gly-BSA or vehicle (bovine serum albumin [BSA]) for up to 48 hours. Gly-BSA dose-dependently increased in situ ROS production (whole-cell dichlorodihydrofluorescein fluorescence), with an optimum effect at 400 microg/mL after 24-hour incubation (152+/-10% versus BSA 100%; P<0.01). Treatment with the NADPH oxidase inhibitor apocynin, a Nox2 (gp91phox) antisense oligonucleotide (Nox2 AS), or the peptide gp91ds-tat significantly reduced Gly-BSA-induced ROS production at 24 hours (68.5+/-2.2%, 61.4+/-8.3%, and 53.2+/-5.4% reduction, respectively). NADPH-dependent activity in cell homogenates was also significantly increased by Gly-BSA at 24 hours (161+/-8% versus BSA) and was inhibited by diphenyleneiodonium, apocynin, NOX2AS, and the protein kinase C inhibitor bisindolylmaleimide I but not by a nitric oxide synthase inhibitor or mitochondrial inhibitors. Furthermore, bisindolylmaleimide I prevented Gly-BSA-stimulated Rac1 translocation, an essential step for NADPH oxidase activation. Gly-BSA-induced increases in ROS were associated with apocynin-inhibitable nuclear translocation of nuclear factor-kappaB and an increase in atrial natriuretic factor mRNA expression. CONCLUSIONS: Gly-BSA stimulates cardiomyocyte ROS production through a protein kinase C-dependent activation of a Nox2-containing NADPH oxidase, which results in nuclear factor-kappaB activation and upregulation of atrial natriuretic factor mRNA. These findings suggest that early-glycated Amadori products may play a role in the development of diabetic heart disease.

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Targets by SciMiner Summary

HUGO ID	Symbol	Target Name	#Occur	ActualStr
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	55	Nox2-containing \| Nox2-Containing \| Nox2-derived \| gp91phox \|
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	44	nadph oxidase \|
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	21	NF-kappaB-dependent \|
7891	NOX4	NADPH oxidase 4	12	Nox4 \| NOX4 \|
399	ALB	albumin	9	albumin \| serum albumin \|
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	8	Rac1 \|
7939	NPPA	natriuretic peptide precursor A	7	ANF \|
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	6	Rac \|
7660	NCF1	neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)	4	p47 \| p47phox \|
2577	CYBA	cytochrome b-245, alpha polypeptide	4	p22phox \| p22 \|
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	3	nitric oxide synthase \|
12805	XDH	xanthine dehydrogenase	3	xanthine oxidase \|
9393	PRKCA	protein kinase C, alpha	3	protein kinase c \|
333	AGT	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	3	angiotensin ii \|
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	2	ap 1 \| AP-1 \|
7661	NCF2	neutrophil cytosolic factor 2 (65kDa, chronic granulomatous disease, autosomal 2)	1	p67 \|
7427	MT-CYB	mitochondrially encoded cytochrome b	1	cytochrome b \|
9802	RAC2	ras-related C3 botulinum toxin substrate 2 (rho family, small GTP binding protein Rac2)	1	Rac2 \|
4823	HBA1	hemoglobin, alpha 1	1	HBA \|
4827	HBB	hemoglobin, beta	1	hemoglobin \|
6025	IL8	interleukin 8	1	NaF \|
6018	IL6	interleukin 6 (interferon, beta 2)	1	interleukin 6 \|
7662	NCF4	neutrophil cytosolic factor 4, 40kDa	1	p40 \|
1784	CDKN1A	cyclin-dependent kinase inhibitor 1A (p21, Cip1)	1	p21 \|

Targets by SciMiner Full list

HUGO ID	Symbol	Name	ActualStr	Score	FlankingText
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Treatment with the NADPH oxidase inhibitor apocynin a Nox2 (gp91phox) gp91phox antisense oligonucleotide (Nox2 Nox2 AS or the peptide
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	gp91phox	2.8	Treatment with the NADPH oxidase inhibitor apocynin a Nox2 (gp91phox) gp91phox antisense oligonucleotide (Nox2 Nox2 AS or the peptide gp91ds-tat significantly
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	oxidase inhibitor apocynin a Nox2 (gp91phox) gp91phox antisense oligonucleotide (Nox2 Nox2 AS or the peptide gp91ds-tat significantly reduced Gly-BSA-induced ROS production
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	Furthermore bisindolylmaleimide I prevented Gly-BSA-stimulated Rac1 translocation an essential step for NADPH oxidase activation
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	ROS production through a protein kinase C-dependent activation of a Nox2-containing NADPH oxidase which results in nuclear factor-kappaB activation and upregulation
4827	HBB	hemoglobin, beta	hemoglobin	1.0	The Amadori adducts or early-glycated products most of which are hemoglobin A 1C (HBA HBA 1C and fructosamine constitute the overwhelming
4823	HBA1	hemoglobin, alpha 1	HBA	1.0	early-glycated products most of which are hemoglobin A 1C (HBA HBA 1C and fructosamine constitute the overwhelming majority of circulating glycated
1784	CDKN1A	cyclin-dependent kinase inhibitor 1A (p21, Cip1)	p21	0.6	membrane-bound cytochrome b 558 (made made up of the subunits p22 and 1 of several NADPH oxidase Nox isoforms
2577	CYBA	cytochrome b-245, alpha polypeptide	p22	0.3	membrane-bound cytochrome b 558 (made made up of the subunits p22 and 1 of several NADPH oxidase Nox isoforms
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	gp91phox	2.8	identified to date the major isoforms expressed in cardiomyocytes are gp91phox (Nox2) Nox2 and Nox4
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	date the major isoforms expressed in cardiomyocytes are gp91phox (Nox2) Nox2 and Nox4
7891	NOX4	NADPH oxidase 4	NOX4	0.9	date the major isoforms expressed in cardiomyocytes are gp91phox (Nox2) Nox2 and Nox4
7891	NOX4	NADPH oxidase 4	Nox4	0.9	major isoforms expressed in cardiomyocytes are gp91phox (Nox2) Nox2 and Nox4
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Whereas Nox2 is regulated by 4 cytosolic subunits (p47 p47 p67 p40
7660	NCF1	neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)	p47	0.3	Whereas Nox2 is regulated by 4 cytosolic subunits (p47 p47 p67 p40 and Rac1 or Rac2 which translocate to the
7662	NCF4	neutrophil cytosolic factor 4, 40kDa	p40	0.3	Nox2 is regulated by 4 cytosolic subunits (p47 p47 p67 p40 and Rac1 or Rac2 which translocate to the membrane on
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	regulated by 4 cytosolic subunits (p47 p47 p67 p40 and Rac1 or Rac2 which translocate to the membrane on enzyme activation
7891	NOX4	NADPH oxidase 4	Nox4	0.9	to the membrane on enzyme activation current evidence suggests that Nox4 is constitutively active and may not require cytosolic subunits for
7661	NCF2	neutrophil cytosolic factor 2 (65kDa, chronic granulomatous disease, autosomal 2)	p67	0.2	Whereas Nox2 is regulated by 4 cytosolic subunits (p47 p47 p67 p40 and Rac1 or Rac2 which translocate to the membrane
9802	RAC2	ras-related C3 botulinum toxin substrate 2 (rho family, small GTP binding protein Rac2)	Rac2	0.1	4 cytosolic subunits (p47 p47 p67 p40 and Rac1 or Rac2 which translocate to the membrane on enzyme activation current evidence
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Furthermore macrophages derived from mice deficient in the Nox2 subunit of NADPH oxidase failed to display enhanced levels of
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Antisense Nox2 and Nox4 Oligonucleotides
7891	NOX4	NADPH oxidase 4	NOX4	0.9	Antisense Nox2 and Nox4 Oligonucleotides
7891	NOX4	NADPH oxidase 4	Nox4	0.9	Antisense Nox2 and Nox4 Oligonucleotides
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Nox2 and Nox4 antisense morpholino oligonucleotides (AS; AS Gene Tools USA
7891	NOX4	NADPH oxidase 4	NOX4	0.9	Nox2 and Nox4 antisense morpholino oligonucleotides (AS; AS Gene Tools USA
7891	NOX4	NADPH oxidase 4	Nox4	0.9	Nox2 and Nox4 antisense morpholino oligonucleotides (AS; AS Gene Tools USA were designed
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	designed on the basis of the published rat sequences of Nox2 cDNA (5'-CCTCATTCACAGCCCAGTTCCCCAT-3') 5'-CCTCATTCACAGCCCAGTTCCCCAT-3' and Nox4 cDNA (5' 5' -CAGCTCCTCCAGGACAGCGCCATAC-3' and
7891	NOX4	NADPH oxidase 4	Nox4	0.9	the published rat sequences of Nox2 cDNA (5'-CCTCATTCACAGCCCAGTTCCCCAT-3') 5'-CCTCATTCACAGCCCAGTTCCCCAT-3' and Nox4 cDNA (5' 5' -CAGCTCCTCCAGGACAGCGCCATAC-3' and correspond to the region near
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	region near the 5' translational start site of the Nox2/4 Nox2 4 open reading frame
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Nox2 protein expression was assessed by Western blot analysis
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Gp91ds is a peptide from cytosolic domain B of Nox2 which interferes with the binding of the cytosolic oxidase subunit
7660	NCF1	neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)	p47	0.3	which interferes with the binding of the cytosolic oxidase subunit p47 with the membrane-bound Nox isoform
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	A scrambled 9-amino acid Nox2 sequence (scrmb-tat) scrmb-tat was used as a control
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	The oligonucleotide primers were as follows atrial natriuretic factor (ANF): ANF forward primer 5'-CCAGGCCATATTGGAGCAAA-3' reverse primer 5'-GCAGGTTCTTGAAATCCATCAG-3' _amp_#223 -actin forward primer
6025	IL8	interleukin 8	NaF	0.3	1 mmol/L mmol L MgCl 2 1 mmol/L mmol L NaF 1 mmol/L mmol L Na 3 VO 4 and protease
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	Rac protein levels were normalized by the p22phox protein level and
2577	CYBA	cytochrome b-245, alpha polypeptide	p22phox	1.3	Rac protein levels were normalized by the p22phox protein level and values expressed in arbitrary units
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	NF-kappaB staining was visualized by DAB substrate (Vector Vector Laboratories
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	The major novel finding of this study is that a Nox2-containing NADPH oxidase is pivotally involved in the oxidative response of
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	ROS production is linked to activation of the transcription factor NF-kappaB and to increased ANF mRNA expression which suggests that Gly-BSA
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	to activation of the transcription factor NF-kappaB and to increased ANF mRNA expression which suggests that Gly-BSA may play a role
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	role in altering the cardiomyocyte phenotype through activation of a Nox2-containing NADPH oxidase
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	production in cardiomyocytes largely via a PKC-mediated activation of a Nox2-containing NADPH oxidase
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	that soluble RAGE was able to inhibit the increases in NF-kappaB and AP-1 activity in response to AGE but not Gly-BSA
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	AP-1	1.0	RAGE was able to inhibit the increases in NF-kappaB and AP-1 activity in response to AGE but not Gly-BSA
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	RT-PCR experiments did not reveal any increase in expression of Nox2 Nox4 p47phox or p22phox after Gly-BSA treatment (data data not
7891	NOX4	NADPH oxidase 4	Nox4	0.9	experiments did not reveal any increase in expression of Nox2 Nox4 p47phox or p22phox after Gly-BSA treatment (data data not shown
7660	NCF1	neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)	p47phox	1.3	did not reveal any increase in expression of Nox2 Nox4 p47phox or p22phox after Gly-BSA treatment (data data not shown
2577	CYBA	cytochrome b-245, alpha polypeptide	p22phox	1.3	reveal any increase in expression of Nox2 Nox4 p47phox or p22phox after Gly-BSA treatment (data data not shown
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Nox2 is a major Nox isoform within the cardiovascular system
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	Our previous results demonstrated a pivotal role for a Nox2-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy and in the
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	To specifically investigate the role of the Nox2 subunit in Gly-BSA-induced ROS production myocytes were pretreated with either
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	pretreated with either an antisense morpholino oligonucleotide that specifically targeted Nox2 or the NADPH oxidase inhibitor gp91ds-tat
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	in vitro an effect thought to be mediated via the Nox2 subunit
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	No significant effect of the Nox2 AS or gp91ds-tat on ROS production was observed under baseline
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	under baseline conditions (data data not shown but both the Nox2 AS and gp91ds-tat significantly attenuated in situ Gly-BSA-induced ROS production
7891	NOX4	NADPH oxidase 4	Nox4	0.9	In contrast treatment with a Nox4 AS had no effect on Gly-BSA-induced ROS production consistent with
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Gly-BSA response originated from the oxidase the ability of the Nox2 AS and apocynin to inhibit the Gly-BSA-induced increase in NADPH-dependent
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Both apocynin and Nox2 AS completely abolished Gly-BSA-induced stimulation of NADPH-dependent superoxide production which
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	stimulation of NADPH-dependent superoxide production which suggests complete inhibition of Nox2 activity
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Thus these experiments suggest that the inability of apocynin and Nox2 AS to completely inhibit Gly-BSA-induced increases in DCF fluorescence (total
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	several studies have demonstrated important roles for both PKC and Rac
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	Another important activator of the NADPH oxidase is Rac
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	that Bis I completely prevented the Gly-BSA-induced membrane translocation of Rac1 which suggests that PKC lies upstream of Rac and oxidase
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	translocation of Rac1 which suggests that PKC lies upstream of Rac and oxidase activation in the signaling pathway that leads to
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	Activation of the transcription factor NF-kappaB is important in the regulation of genes in response to
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	NF-kappaB is recognized as an important redox-sensitive transcription factor and has
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	We have demonstrated that Gly-BSA stimulates translocation of NF-kappaB to the nucleus and that apocynin can almost completely inhibit
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	Furthermore apocynin or gp91ds-tat completely inhibited the increase in NF-kappaB activity induced by Gly-BSA
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-derived	2.8	Collectively these data strongly suggest that Nox2-derived ROS plays an important role in Gly-BSA-induced NF-kappaB activation
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	suggest that Nox2-derived ROS plays an important role in Gly-BSA-induced NF-kappaB activation
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	In line with an important role for NF-kappaB in the development of cardiac hypertrophy ANF mRNA expression was
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	important role for NF-kappaB in the development of cardiac hypertrophy ANF mRNA expression was stimulated to a similar degree by Gly-BSA
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	via the production of ROS and subsequent downstream activation of NF-kappaB and redox-sensitive genes
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	These effects involve the specific activation of a Nox2-containing NADPH oxidase
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	A Translocation of Rac by Gly-BSA
391	AKT1	v-akt murine thymoma viral oncogene homolog 1	Rac	0.5	Cells were stained with anti-Rac1 monoclonal antibody arrows indicate Rac translocation to the plasma membrane
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	B Western blot analysis of membrane Rac1 protein expression ** P _lt_0.01 vs BSA control P _lt_0.01
2577	CYBA	cytochrome b-245, alpha polypeptide	p22	0.0	vs BSA control P _lt_0.01 vs Gly-BSA n=4/group n=4 group p22 was used an internal loading control
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	A Nox2-containing NADPH oxidase is involved in Gly-BSA-induced ROS production
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	A Effect of Nox2 AS on Nox2 protein expression by immunoblotting
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	A Effect of Nox2 AS on Nox2 protein expression by immunoblotting
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	EPEI oligo delivery reagent SC scrambled control oligo AS antisense Nox2 morpholino oligonucleotide and Nox2 protein from Nox2 mouse as negative
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	SC scrambled control oligo AS antisense Nox2 morpholino oligonucleotide and Nox2 protein from Nox2 mouse as negative control
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	oligo AS antisense Nox2 morpholino oligonucleotide and Nox2 protein from Nox2 mouse as negative control
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	B Effect of Nox2 AS on Gly-BSA (400 400 microg/mL, microg mL 24 hours
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	of apocynin (Apo; Apo 500 micromol/L) micromol L and antisense Nox2 on Gly-BSA-induced NADPH oxidase activity ** P _lt_0.01 vs control
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	A Activation of NF-kappaB by Gly-BSA
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	B Western blot analysis of nuclear NF-kappaB protein expression
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	of Gly-BSA (400 400 microg/mL, microg mL 24 hours on ANF mRNA expression ** P _lt_0.01 vs BSA control P _lt_0.05
7660	NCF1	neutrophil cytosolic factor 1, (chronic granulomatous disease, autosomal 1)	p47	0.3	Apocynin prevents the association of the cytosolic subunit p47 with the membrane-bound catalytic subunit of NADPH oxidase
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	by immunofluorescence experiments demonstrating a clearly increased membrane translocation of Rac1 in cardiomyocytes pretreated for 24 hours with Gly-BSA ( Figure
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	This increase in membrane translocation of Rac1 is completely lost in the presence of Bis I Confirmation
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	A significantly increased membrane expression of Rac1 was observed in the presence of Gly-BSA that was prevented
9801	RAC1	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Rac1	0.5	results suggest that PKC is required for the translocation of Rac1 to the plasma membrane in the presence of Gly-BSA
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-Containing	2.8	Role of a Nox2-Containing NADPH Oxidase in Gly-BSA-Induced ROS Production
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Nox2 is one of the major Nox isoforms of NADPH oxidase
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	To investigate the role of Nox2 in Gly-BSA-induced ROS production myocytes were pretreated with an antisense
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	pretreated with an antisense morpholino oligonucleotide that specifically targeted the Nox2 subunit (Nox2 Nox2 AS
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	antisense morpholino oligonucleotide that specifically targeted the Nox2 subunit (Nox2 Nox2 AS
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Treatment of neonatal myocytes with the Nox2 AS markedly decreased Nox2 protein expression 48 hours after treatment
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Treatment of neonatal myocytes with the Nox2 AS markedly decreased Nox2 protein expression 48 hours after treatment ( Figure 5 A
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	In line with this the Nox2 AS also significantly attenuated Gly-BSA-induced in situ ROS production in
7891	NOX4	NADPH oxidase 4	Nox4	0.9	A Nox4 AS also had no effect on Gly-BSA-induced ROS production (Gly-BSA
7891	NOX4	NADPH oxidase 4	Nox4	0.9	Gly-BSA-induced ROS production (Gly-BSA Gly-BSA 158_amp_#177 6% versus Gly-BSA plus Nox4 AS 160_amp_#177 3%
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	For further corroboration of the Nox2 AS results neonatal myocytes were treated with the NADPH oxidase
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	In line with the effect of the Nox2 AS gp91ds-tat (20 20 micromol/L) micromol L significantly attenuated Gly-BSA-induced
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	Preincubation with either apocynin or Nox2 AS completely abolished Gly-BSA-induced stimulation of NADPH oxidase activity (
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	of the Gly-BSA-induced increase in DCF fluorescence by apocynin and Nox2 AS may be because only 50% to 60% of this
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	only 50% to 60% of this ROS originates from a Nox2-containing oxidase
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2-containing	2.8	These experiments collectively strongly support the concept that a Nox2-containing NADPH oxidase is a major source of Gly-BSA-induced ROS production
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	Activation of NF-kappaB and ANF mRNA Expression
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	Activation of NF-kappaB and ANF mRNA Expression
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	In its inactive state NF-kappaB is maintained as a latent form present in the cytoplasm
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	400 microg/mL microg mL Gly-BSA for 24 hours resulted in NF-kappaB activation as depicted by enhanced translocation of NF-kappaB to the
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	resulted in NF-kappaB activation as depicted by enhanced translocation of NF-kappaB to the nucleus ( Figure 6 A
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	with anti-NF-kappaB antibody revealed a consistently increased level of nuclear NF-kappaB expression after Gly-BSA incubation for 24 hours (2.30_amp_#177;0.42-fold 2.30_amp_#177 0.42-fold
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	Apocynin significantly inhibited NF-kappaB nuclear translocation
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	To further confirm these data we additionally analyzed NF-kappaB activity using an NF-kappaB-dependent promoter luciferase reporter assay
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB-dependent	0.6	confirm these data we additionally analyzed NF-kappaB activity using an NF-kappaB-dependent promoter luciferase reporter assay
7794	NFKB1	nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)	NF-kappaB	0.6	Associated with NF-kappaB activation was a significant increase in mRNA expression of the
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	a significant increase in mRNA expression of the hypertrophic marker ANF (2.76_amp_#177;0.48-fold 2.76_amp_#177 0.48-fold increase versus BSA controls Figure 6 C
7939	NPPA	natriuretic peptide precursor A	ANF	2.6	and apocynin significantly inhibited this increase which suggests that Gly-BSA-stimulated ANF expression was redox-sensitive and occurred via NADPH oxidase activation
2578	CYBB	cytochrome b-245, beta polypeptide (chronic granulomatous disease)	Nox2	4.6	F Wientjes University College London London United Kingdom for the Nox2 antibody
399	ALB	albumin	serum albumin	1.0	however the effects of early glycated proteins such as glycated serum albumin gly bsa are poorly defined.
399	ALB	albumin	serum albumin	1.0	methods and results_amp_#151; cultured neonatal rat cardiomyocytes were incubated with gly bsa or vehicle bovine serum albumin [bsa] for up to 48 hours.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	treatment with the nadph oxidase inhibitor apocynin a nox2 gp91phox antisense oligonucleotide nox2 as or the peptide gp91ds tat significantly reduced gly bsa induced ros production at 24 hours 68.5_amp_#177;2.2% 61.4_amp_#177;8.3% a
9393	PRKCA	protein kinase C, alpha	protein kinase c	1.0	nadph dependent activity in cell homogenates was also significantly increased by gly bsa at 24 hours 161_amp_#177;8% versus bsa and was inhibited by diphenyleneiodonium apocynin nox2as and the protein kinase c inhibitor bisindolylmaleimide i but not by a nitric oxide synthase inhibitor or mitochondrial inhibitors.
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	nitric oxide synthase	1.0	ignificantly increased by gly bsa at 24 hours 161_amp_#177;8% versus bsa and was inhibited by diphenyleneiodonium apocynin nox2as and the protein kinase c inhibitor bisindolylmaleimide i but not by a nitric oxide synthase inhibitor or mitochondrial inhibitors.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	furthermore bisindolylmaleimide i prevented gly bsa stimulated rac1 translocation an essential step for nadph oxidase activation.
9393	PRKCA	protein kinase C, alpha	protein kinase c	1.0	conclusions_amp_#151; gly bsa stimulates cardiomyocyte ros production through a protein kinase c dependent activation of a nox2 containing nadph oxidase which results in nuclear factor kappab activation and upregulation of atrial natriuretic factor mrna.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	conclusions_amp_#151; gly bsa stimulates cardiomyocyte ros production through a protein kinase c dependent activation of a nox2 containing nadph oxidase which results in nuclear factor kappab activation and upregulation of atrial natriuretic factor mrna.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	key words: glycation _amp_#149; nadph oxidase _amp_#149; free radicals _amp_#149; glucose _amp_#149; diabetes mellitus
399	ALB	albumin	albumin	1.0	in type i diabetic patients amadori albumin was increased approximately 2 fold and was correlated with markers of endothelial vascular dysfunction as well as with early nephropathy and with retinopathy status.
399	ALB	albumin	albumin	1.0	furthermore previous studies have demonstrated that antiglycated albumin therapy prevented nephropathy and retinopathy in diabetic mice.
399	ALB	albumin	serum albumin	1.0	in vascular smooth muscle cells glycated serum albumin resulted in a significant stimulation of proliferation and migration as well as nuclear factor nf kappab activation which led to the induction of monocyte chemoattractant factor and interleukin 6.
6018	IL6	interleukin 6 (interferon, beta 2)	interleukin 6	1.0	ted serum albumin resulted in a significant stimulation of proliferation and migration as well as nuclear factor nf kappab activation which led to the induction of monocyte chemoattractant factor and interleukin 6.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	although multiple ros sources are implicated in diabetes a major source that is important in diabetic vascular disease is nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	the latter is a multisubunit complex that consists of a membrane bound cytochrome b 558 made up of the subunits p22 and 1 of several nadph oxidase [nox] isoforms .
7427	MT-CYB	mitochondrially encoded cytochrome b	cytochrome b	1.0	the latter is a multisubunit complex that consists of a membrane bound cytochrome b 558 made up of the subunits p22 and 1 of several nadph oxidase [nox] isoforms .
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	h ages induced intracellular generation of hydrogen peroxide which was inhibited by the flavoprotein inhibitor diphenyleneiodonium dpi but not by inhibitors of nitric oxide consistent with a role for nadph oxidase in this process.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	furthermore macrophages derived from mice deficient in the nox2 subunit of nadph oxidase failed to display enhanced levels of tissue factor on stimulation with age.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	interestingly recent studies indicate an important role for ros production particularly that derived from nadph oxidase in both angiotensin ii induced and pressure overload induced cardiac hypertrophy.
333	AGT	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	angiotensin ii	1.0	interestingly recent studies indicate an important role for ros production particularly that derived from nadph oxidase in both angiotensin ii induced and pressure overload induced cardiac hypertrophy.
399	ALB	albumin	serum albumin	1.0	the aim of the present study was to investigate the effects of glycated serum albumin on ros production in cardiomyocytes to identify the potential sources of ros production and to assess the downstream effects of ros generation.
399	ALB	albumin	serum albumin	1.0	bovine serum albumin bsa; nonglycated and glycated was obtained from sigma chemical co.
399	ALB	albumin	albumin	1.0	the procedure 4 to 5 days' incubation in 28 mmol/l glucose at 25degreec used to synthesize glycated albumin gly bsa generates amadori glucose adducts with little or no oxidative degradation products or formation of age.
399	ALB	albumin	albumin	1.0	nonglycated bsa was used as a control such that each control well was exposed to an albumin concentration equivalent to that of the treated wells.
9393	PRKCA	protein kinase C, alpha	protein kinase c	1.0	subsets of myocytes were also exposed to the antioxidants n acetylcysteine nac; 10 mmol/l or butylated hydroxyanisole bha; 50 micromol/l the nadph oxidase inhibitor apocynin 500 micromol/l the protein kinase c pkc inhibitor bisindolylmaleimide i bis i; 5 micromol/l a rabbit anti human anti rage receptor for age antibody 75 microg/ml or appropriate vehicle for 1 hour before bsa gly bsa or age treatment.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	subsets of myocytes were also exposed to the antioxidants n acetylcysteine nac; 10 mmol/l or butylated hydroxyanisole bha; 50 micromol/l the nadph oxidase inhibitor apocynin 500 micromol/l the protein kinase c pkc inhibitor bisindolylmaleimide i bis i; 5 micromol/l a rabbit anti human anti rage receptor for age antibody 75 microg/ml or appropriate vehi
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	the following agents were used to assess potential sources of o 2 production: dpi a flavoprotein inhibitor 10 micromol/l ; apocynin an nadph oxidase inhibitor 500 micromol/l ; the cell permeable superoxide scavenger tiron 4 5 dihydroxy 1 3 benzene disulfonic acid; 20 mmol/l ; the nitric oxide synthase inhibitor l name n nitro l arginine methyl es
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	nitric oxide synthase	1.0	a flavoprotein inhibitor 10 micromol/l ; apocynin an nadph oxidase inhibitor 500 micromol/l ; the cell permeable superoxide scavenger tiron 4 5 dihydroxy 1 3 benzene disulfonic acid; 20 mmol/l ; the nitric oxide synthase inhibitor l name n nitro l arginine methyl ester; 100 micromol/l ; the xanthine oxidase inhibitor allopurinol 100 micromol/l ; the complex i mitochondrial electron chain inhibitor rotenone 2 micromol
12805	XDH	xanthine dehydrogenase	xanthine oxidase	1.0	; the cell permeable superoxide scavenger tiron 4 5 dihydroxy 1 3 benzene disulfonic acid; 20 mmol/l ; the nitric oxide synthase inhibitor l name n nitro l arginine methyl ester; 100 micromol/l ; the xanthine oxidase inhibitor allopurinol 100 micromol/l ; the complex i mitochondrial electron chain inhibitor rotenone 2 micromol/l ; the complex ii mitochondrial electron chain inhibitor thenoyltrifluroacetone 10 mic
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	the major novel finding of this study is that a nox2 containing nadph oxidase is pivotally involved in the oxidative response of isolated cardiomyocytes to glycated albumin.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	of the transcription factor nf kappab and to increased anf mrna expression which suggests that gly bsa may play a role in altering the cardiomyocyte phenotype through activation of a nox2 containing nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	the present study provides strong evidence that an early glycated protein stimulates ros production in cardiomyocytes largely via a pkc mediated activation of a nox2 containing nadph oxidase.
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	ap 1	1.0	similarly hattori et al also demonstrated in vascular smooth muscle cells that soluble rage was able to inhibit the increases in nf kappab and ap 1 activity in response to age but not gly bsa.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	our previous results demonstrated a pivotal role for a nox2 containing nadph oxidase in angiotensin ii induced cardiac hypertrophy and in the response of the macrophage to age.
333	AGT	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	angiotensin ii	1.0	our previous results demonstrated a pivotal role for a nox2 containing nadph oxidase in angiotensin ii induced cardiac hypertrophy and in the response of the macrophage to age.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	ifically investigate the role of the nox2 subunit in gly bsa induced ros production myocytes were pretreated with either an antisense morpholino oligonucleotide that specifically targeted nox2 or the nadph oxidase inhibitor gp91ds tat.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	gp91ds tat has been shown to completely block angiotensin ii induced aortic nadph oxidase activity both in vivo and in vitro an effect thought to be mediated via the nox2 subunit.
333	AGT	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	angiotensin ii	1.0	gp91ds tat has been shown to completely block angiotensin ii induced aortic nadph oxidase activity both in vivo and in vitro an effect thought to be mediated via the nox2 subunit.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	however it failed to attenuate either potassium superoxide or xanthine oxidase generated superoxide which indicates specificity for the nadph oxidase.
12805	XDH	xanthine dehydrogenase	xanthine oxidase	1.0	however it failed to attenuate either potassium superoxide or xanthine oxidase generated superoxide which indicates specificity for the nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	activation of nadph oxidase occurs via multiple signaling pathways ; however several studies have demonstrated important roles for both pkc and rac.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	in the present study the nonspecific pkc inhibitor bis i dpi and tiron prevented the gly bsa stimulation of nadph oxidase activity.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	this suggests that pkc does not tonically stimulate nadph oxidase activity.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	another important activator of the nadph oxidase is rac.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	hyperglycemia has been shown to stimulate ros production in a range of cell types from both mitochondrial sources and nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	an involvement of the oxidase was supported by a significant stimulation of nadph oxidase activity at 24 hours and by the fact that apocynin reduced intracellular ros production after hg treatment by _amp_50% data not shown .
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	thus these results suggest that in cardiomyocytes hg stimulates ros production modestly and slowly and that a significant portion of this response is attributable to nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	these results are in line with those of basta et al who recently reported that age induced ros generation in endothelial cells originates from both nadph oxidase and mitochondria.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	these effects involve the specific activation of a nox2 containing nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	gly bsa induced ros production occurs via pkc dependent activation of nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	a nox2 containing nadph oxidase is involved in gly bsa induced ros production.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	d effects of apocynin apo; 500 micromol/l and antisense nox2 on gly bsa induced nadph oxidase activity. ** p _lt_0.01 vs control; p _lt_0.01 vs gly bsa.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	gly bsa induced ros production occurs via a pkc dependent activation of nadph oxidase
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	apocynin was used to determine the involvement of nadph oxidase in gly bsa induced ros production.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	apocynin prevents the association of the cytosolic subunit p47 with the membrane bound catalytic subunit of nadph oxidase.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	thus to further clarify the involvement of the oxidase the effect of gly bsa on nadph oxidase activity was specifically assessed by lucigenin enhanced chemiluminescence with nadph as a substrate in cardiomyocyte homogenates.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	figure 3 b clearly demonstrates that gly bsa significantly increased nadph oxidase activity by 61_amp_#177;8% p _lt_0.01; n=5 and that this increase was completely blocked by the flavoprotein inhibitor dpi the cell permeable superoxide scavenger tiron and the pkc inhibitor bis i 5
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	further experiments demonstrated that bis i alone had no significant effect on nadph oxidase activity data not shown .
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	nitric oxide synthase	1.0	importantly ros production was unaffected by a range of mitochondrial inhibitors a nitric oxide synthase inhibitor or a xanthine oxidase inhibitor.
12805	XDH	xanthine dehydrogenase	xanthine oxidase	1.0	importantly ros production was unaffected by a range of mitochondrial inhibitors a nitric oxide synthase inhibitor or a xanthine oxidase inhibitor.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	further information regarding the mechanism by which pkc activates nadph oxidase is provided by immunofluorescence experiments demonstrating a clearly increased membrane translocation of rac1 in cardiomyocytes pretreated for 24 hours with gly bsa figure 4 a .
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	role of a nox2 containing nadph oxidase in gly bsa induced ros production
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	nox2 is one of the major nox isoforms of nadph oxidase expressed in cardiomyocytes.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	for further corroboration of the nox2 as results neonatal myocytes were treated with the nadph oxidase inhibitor gp91ds tat.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	lucigenin enhanced chemiluminescence was used to specifically assess the effect of the oxidase inhibitors on gly bsa induced nadph oxidase activity.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	preincubation with either apocynin or nox2 as completely abolished gly bsa induced stimulation of nadph oxidase activity figure 5 d .
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	these experiments collectively strongly support the concept that a nox2 containing nadph oxidase is a major source of gly bsa induced ros production.
14874	NOX5	NADPH oxidase, EF-hand calcium binding domain 5	nadph oxidase	1.0	both nac and apocynin significantly inhibited this increase which suggests that gly bsa stimulated anf expression was redox sensitive and occurred via nadph oxidase activation.