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PMID	16753239 ( )
Title	Peroxisome proliferator-activated receptor agonist regulation of glial activation: relevance to CNS inflammatory disorders.
Abstract	Peroxisome proliferator-activated receptors (PPARs) play key roles in lipid metabolism and inflammation. Recent studies indicated that PPARs are also capable of modulating immune responses. Microglia and astrocytes are cells resident to the central nervous system (CNS) that function to protect against environmental insults including pathogens. However, following CNS inflammation, reactive gliosis occurs which is characterized by astrocyte hypertrophy and increased glial proliferation. Under such conditions, glia can become chronically activated and may contribute to the neuropathology associated with a variety of neuroinflammatory disorders including multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and stroke. A review of the role of PPAR agonists in modulating glial cell activation is presented. Included is a discussion of the molecular mechanisms of action of these PPAR agonists and the potential utility of these agents for the treatment of neuroinflammatory disorders. Arkansas for Medical Sciences, Little Rock, AR 72205, USA. drewpauld @uams.edu

NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.

Targets by SciMiner Summary

HUGO ID	Symbol	Target Name	#Occur	ActualStr
9236	PPARG	peroxisome proliferator-activated receptor gamma	72	PPAR-G \|
9232	PPARA	peroxisome proliferator-activated receptor alpha	46	PPAR \| PPAR-A \| PPARs \|
6018	IL6	interleukin 6 (interferon, beta 2)	14	IL-6 \| il 6 \|
9235	PPARD	peroxisome proliferator-activated receptor delta	9	PPAR-B \|
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	9	TNF-A \|
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	6	APP \| amyloid \|
10618	CCL2	chemokine (C-C motif) ligand 2	6	mcp 1 \| MCP-1 \|
11362	STAT1	signal transducer and activator of transcription 1, 91kDa	4	STAT1 \| STAT-1 \|
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	4	iNOS \|
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	4	ap 1 \| AP-1 \|
1705	CD86	CD86 molecule	4	CD86 \|
1700	CD80	CD80 molecule	2	CD80 \|
19383	SOCS1	suppressor of cytokine signaling 1	2	socs 1 \| suppressor of cytokine signaling 1 \|
15531	EBNA1BP2	EBNA1 binding protein 2	2	p40 \|
11782	TH	tyrosine hydroxylase	2	tyrosine hydroxylase \|
6192	JAK2	Janus kinase 2 (a protein tyrosine kinase)	2	JAK2 \|
11919	CD40	CD40 molecule, TNF receptor superfamily member 5	2	CD40 \|
5962	IL10	interleukin 10	2	IL-10 \| il 10 \|
1984	CISH	cytokine inducible SH2-containing protein	2	suppressor of cytokine signaling \| SOCS \|
6014	IL4	interleukin 4	2	IL-4 \| il 4 \|
11364	STAT3	signal transducer and activator of transcription 3 (acute-phase response factor)	2	stat3 \| STAT3 \|
9605	PTGS2	prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)	2	COX-2 \| cox 2 \|
4931	HLA-A	major histocompatibility complex, class I, A	1	MHC \|
10477	RXRA	retinoid X receptor, alpha	1	retinoid x receptor \|
8975	PIK3CA	phosphoinositide-3-kinase, catalytic, alpha polypeptide	1	phosphatidylinositol 3 kinase \|
3133	EBP	emopamil binding protein (sterol isomerase)	1	EBP-_amp_#x3b2 \|
6925	MBP	myelin basic protein	1	myelin basic protein \|
6190	JAK1	Janus kinase 1 (a protein tyrosine kinase)	1	JAK1 \|
613	APOE	apolipoprotein E	1	apolipoprotein e \|
5438	IFNG	interferon, gamma	1	IFN-G \|
1678	CD4	CD4 molecule	1	CD4 \|
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	1	superoxide dismutase 1 \|

Targets by SciMiner Full list

HUGO ID	Symbol	Name	ActualStr	Score	FlankingText
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Peroxisome proliferator-activated receptors (PPARs) PPARs play key roles in lipid metabolism and inflammation
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Recent studies indicated that PPARs are also capable of modulating immune responses
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	A review of the role of PPAR agonists in modulating glial cell activation is presented
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	a discussion of the molecular mechanisms of action of these PPAR agonists and the potential utility of these agents for the
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Peroxisome proliferator-activated receptors (PPARs) PPARs are members of a superfamily of proteins termed nuclear receptors
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	The role of PPARs in regulating the transcription of genes involved in glucose and
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	Three major subtypes of PPAR exist which are designated PPAR-_amp_#x3b1 -_amp_#x3b2;/_amp_#x3b4;, -_amp_#x3b2 _amp_#x3b4 and -_amp_#x3b3
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Three major subtypes of PPAR exist which are designated PPAR-_amp_#x3b1 -_amp_#x3b2;/_amp_#x3b4;, -_amp_#x3b2 _amp_#x3b4 and -_amp_#x3b3
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	commonly prescribed for the treatment of type II diabetes are PPAR-_amp_#x3b3 ligands
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Naturally occurring PPAR-_amp_#x3b3 ligands include eicosanoids polyunsaturated fatty acids and the cyclopentenone prostaglandin
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	NSAID including indomethacin which are used to treat inflammation are PPAR-_amp_#x3b3 ligands
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	These observations stimulated studies investigating the role of PPAR in modulating inflammation
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Critical early studies in this field demonstrated that PPAR-_amp_#x3b3 agonists are capable of suppressing immune activation of monocyte/macrophages monocyte
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	PPAR-_amp_#x3b1 ligands include fibrates that are commonly used for the treatment
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	acid eicosapentanoic acid and linoleic acid are endogenous ligands for PPAR-_amp_#x3b1 while WY 14 643 and GW7647 are synthetic agonists of
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists include various fatty acids including bromopalmitate the prostacyclin
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	PPARs are capable of regulating gene expression through multiple mechanisms
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	PPARs generally function as heterodimers in association with retinoid-X-receptors (RXRs) RXRs
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	In addition through a mechanism termed receptor-dependent transrepression PPARs are also capable of regulating gene expression independent of binding
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	In addition PPAR interaction with transcriptional co-activator/co-repressor co-activator co-repressor molecules that are in
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 agonists are believed to suppress immune responses principally through transrepression
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	AP-1	1.0	For example these agonists inhibit transcription factors including NF-_amp_#x3ba B AP-1 and STAT-1 from activating gene expression in this manner
11362	STAT1	signal transducer and activator of transcription 1, 91kDa	STAT-1	0.5	these agonists inhibit transcription factors including NF-_amp_#x3ba B AP-1 and STAT-1 from activating gene expression in this manner
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The PPAR-_amp_#x3b3 agonist 15d-PGJ 2 can regulate gene expression through receptor-independent mechanisms
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	PPAR-_amp_#x3b1 agonists also inhibit NF-_amp_#x3ba B activity by inducing the expression
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Effects of PPARs on glial cell activation
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The PPAR-_amp_#x3b3 agonist 15d-PGJ 2 was demonstrated to inhibit NO IL-1_amp_#x3b2 and
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.0	agonist 15d-PGJ 2 was demonstrated to inhibit NO IL-1_amp_#x3b2 and TNF-_amp_#x3b1 production by the BV-2 mouse microglial cell line ( Koppal
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The PPAR-_amp_#x3b3 agonist troglitazone did not suppress the expression of these pro-inflammatory
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	by BV-2 cells suggesting that 15d-PGJ 2 may act through PPAR-_amp_#x3b3 -independent mechanisms ( Petrova et al. 1999
4931	HLA-A	major histocompatibility complex, class I, A	MHC	0.3	al. 2000 demonstrated that 15d-PGJ 2 suppressed TNF-_amp_#x3b1 NO and MHC class II expression by primary rat microglia
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.0	( Bernardo et al. 2000 demonstrated that 15d-PGJ 2 suppressed TNF-_amp_#x3b1 NO and MHC class II expression by primary rat microglia
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	However since the PPAR-_amp_#x3b3 agonist ciglitazone suppressed the production of these pro-inflammatory molecules in
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	similar manner 15d-PGJ 2 was interpreted to act through a PPAR-_amp_#x3b3 dependent mechanism
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	In these studies HCT1026 activated the PPAR-_amp_#x3b3 receptor in microglia and the PPAR-_amp_#x3b3 antagonist GW9662 blocked receptor
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	studies HCT1026 activated the PPAR-_amp_#x3b3 receptor in microglia and the PPAR-_amp_#x3b3 antagonist GW9662 blocked receptor activation ( Bernardo et al. 2005
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The basis for the discrepancy between these studies concerning whether PPAR-_amp_#x3b3 agonists influence microglial cell function through PPAR-_amp_#x3b3 -dependent or -independent
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	studies concerning whether PPAR-_amp_#x3b3 agonists influence microglial cell function through PPAR-_amp_#x3b3 -dependent or -independent mechanisms may be explained by the fact
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	conducted with BV-2 microglial cells which express little or no PPAR-_amp_#x3b3
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	15d-PGJ 2 inhibited NO as well as the cytokines IL-1_amp_#x3b2 IL-6 and TNF-_amp_#x3b1 and the chemokine MCP-1 by both primary mouse
10618	CCL2	chemokine (C-C motif) ligand 2	MCP-1	1.3	as the cytokines IL-1_amp_#x3b2 IL-6 and TNF-_amp_#x3b1 and the chemokine MCP-1 by both primary mouse microglia and astrocytes ( Storer et
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.1	inhibited NO as well as the cytokines IL-1_amp_#x3b2 IL-6 and TNF-_amp_#x3b1 and the chemokine MCP-1 by both primary mouse microglia and
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	molecules in spite of the fact that this agonist binds PPAR-_amp_#x3b3 with lower affinity than thiazolidinediones
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	RA may inhibit cell activation through the formation of PPAR-_amp_#x3b3;/RXR PPAR-_amp_#x3b3 RXR heterodimers
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The expression of PPAR-_amp_#x3b3 increases in microglia and astrocytes during EAE supporting a role
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	is a cyclopentenone prostaglandin but is not believed to bind PPAR-_amp_#x3b3 is a potent inhibitor of the activation of primary mouse
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	suggest that 15d-PGJ 2 likely inhibits glial cell activation by PPAR-_amp_#x3b3 -dependent as well as PPAR-_amp_#x3b3 -independent mechanisms
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	inhibits glial cell activation by PPAR-_amp_#x3b3 -dependent as well as PPAR-_amp_#x3b3 -independent mechanisms
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 agonists are capable of inhibiting inflammatory responses in glia through
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2004) 2004 demonstrated that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 inhibited LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	15d-PGJ 2 inhibited LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 and IL-6 in primary astrocytes
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.0	the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 inhibited LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 and IL-6 in primary astrocytes
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Over expression of wild-type and dominant-negative constructs of PPAR-_amp_#x3b3 or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	expression of wild-type and dominant-negative constructs of PPAR-_amp_#x3b3 or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and iNOS expression in
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	1.5	or the PPAR-_amp_#x3b3 antagonist GW9662 did not alter NO and iNOS expression in these cells
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2003) 2003 demonstrated that the PPAR-_amp_#x3b3 agonists 15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1
11362	STAT1	signal transducer and activator of transcription 1, 91kDa	STAT1	0.5	PPAR-_amp_#x3b3 agonists 15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1 STAT3 JAK1 and JAK2 in microglia and astrocytes
6190	JAK1	Janus kinase 1 (a protein tyrosine kinase)	JAK1	0.3	15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1 STAT3 JAK1 and JAK2 in microglia and astrocytes
6192	JAK2	Janus kinase 2 (a protein tyrosine kinase)	JAK2	0.3	15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1 STAT3 JAK1 and JAK2 in microglia and astrocytes
6192	JAK2	Janus kinase 2 (a protein tyrosine kinase)	JAK2	0.3	and rosiglitazone inhibit the phosphorylation of STAT1 STAT3 JAK1 and JAK2 in microglia and astrocytes
11364	STAT3	signal transducer and activator of transcription 3 (acute-phase response factor)	STAT3	0.4	agonists 15d-PGJ 2 and rosiglitazone inhibit the phosphorylation of STAT1 STAT3 JAK1 and JAK2 in microglia and astrocytes
1984	CISH	cytokine inducible SH2-containing protein	SOCS	1.6	agonists induce the expression of suppressor of cytokine signaling (SOCS) SOCS 1 and 3 which alters JAK/STAT JAK STAT phosphorylation and
11362	STAT1	signal transducer and activator of transcription 1, 91kDa	STAT	0.5	signaling (SOCS) SOCS 1 and 3 which alters JAK/STAT JAK STAT phosphorylation and JAK/STAT JAK STAT mediated signaling
11362	STAT1	signal transducer and activator of transcription 1, 91kDa	STAT	0.5	3 which alters JAK/STAT JAK STAT phosphorylation and JAK/STAT JAK STAT mediated signaling
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 agonist suppression of glial activation can have profound effects on
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	(2000) 2000 demonstrated that conditioned media from _amp_#x3b2 -amyloid treated primary mouse microglia was toxic to mouse cortical neurons
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	However troglitazone treatment of microglia suppressed _amp_#x3b2 -amyloid mediated neuron cell death
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	These studies further demonstrated that a variety of PPAR-_amp_#x3b3 agonists including TZDs 15d-PGJ 2 and NSAIDS blocked _amp_#x3b2 -amyloid
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	PPAR-_amp_#x3b3 agonists including TZDs 15d-PGJ 2 and NSAIDS blocked _amp_#x3b2 -amyloid induction of neurotoxic molecules by monocytes
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	For example these PPAR-_amp_#x3b3 agonists blocked TNF-_amp_#x3b1 and IL-6 expression by monocytes
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	For example these PPAR-_amp_#x3b3 agonists blocked TNF-_amp_#x3b1 and IL-6 expression by monocytes
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.1	For example these PPAR-_amp_#x3b3 agonists blocked TNF-_amp_#x3b1 and IL-6 expression by monocytes
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Collectively this study demonstrated that PPAR-_amp_#x3b3 agonists suppress the production by monocyte/microglial monocyte microglial cells of
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	by studies utilizing rat cortical neuron-glial co-cultures that indicated that PPAR-_amp_#x3b3 agonists including TZDs and 15d-PGJ 2 suppressed LPS induction of
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Interestingly the PPAR-_amp_#x3b1 agonists clofibrate and WY14 643 did not protect neurons in
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	1.5	Recent studies demonstrated that TZDs block the production of iNOS TNF-_amp_#x3b1 IL-6 and COX-2 by primary rat microglia and astrocytes
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	studies demonstrated that TZDs block the production of iNOS TNF-_amp_#x3b1 IL-6 and COX-2 by primary rat microglia and astrocytes and protected
9605	PTGS2	prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)	COX-2	1.0	that TZDs block the production of iNOS TNF-_amp_#x3b1 IL-6 and COX-2 by primary rat microglia and astrocytes and protected cortical neurons
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.4	Recent studies demonstrated that TZDs block the production of iNOS TNF-_amp_#x3b1 IL-6 and COX-2 by primary rat microglia and astrocytes and
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	A PPAR-_amp_#x3b3 antagonist blocked TZD protection of cortical neurons in these studies
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Interestingly PPARs including PPAR-_amp_#x3b3 can be expressed by neurons ( Cimini et
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Interestingly PPARs including PPAR-_amp_#x3b3 can be expressed by neurons ( Cimini et al. 2005
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	Furthermore it has been suggested that PPAR activation in neurons may directly influence neuron cell viability and
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	are required to more definitively determine the mechanisms by which PPAR-_amp_#x3b3 agonists modulate inflammatory responses in the CNS
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	or receptor-independent mechanisms are complicated by the paucity of specific PPAR-_amp_#x3b3 agonists and the fact that PPAR-_amp_#x3b3 -deficient mice die soon
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	the paucity of specific PPAR-_amp_#x3b3 agonists and the fact that PPAR-_amp_#x3b3 -deficient mice die soon after birth
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	In addition PPAR-_amp_#x3b3 agonists have been demonstrated in some studies to function through
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	but receptor-independent mechanisms at higher concentrations perhaps by activating other PPARs ( Welch et al. 2003
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The development of highly selective PPAR-_amp_#x3b3 antagonists and conditional PPAR-_amp_#x3b3 deficient mouse strains will be essential
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The development of highly selective PPAR-_amp_#x3b3 antagonists and conditional PPAR-_amp_#x3b3 deficient mouse strains will be essential in determining the mechanisms
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	strains will be essential in determining the mechanisms by which PPAR-_amp_#x3b3 agonists control CNS inflammation
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	PPAR-_amp_#x3b1
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Relatively few studies have investigated the effects of PPAR-_amp_#x3b1 agonists on glial cell activation
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	(2002) 2002 demonstrated that the PPAR-_amp_#x3b1 agonist gemfibrozil inhibited cytokine induction of NO and iNOS by
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	1.5	the PPAR-_amp_#x3b1 agonist gemfibrozil inhibited cytokine induction of NO and iNOS by human astroglial and primary astrocytes
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Gemfibrozil was suggested to function in a PPAR-_amp_#x3b1 independent manner in these studies since a dominant negative PPAR-_amp_#x3b1
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	PPAR-_amp_#x3b1 independent manner in these studies since a dominant negative PPAR-_amp_#x3b1 mutant did not overcome gemfibrozil mediated inhibition of iNOS gene
7873	NOS2A	nitric oxide synthase 2A (inducible, hepatocytes)	iNOS	1.5	negative PPAR-_amp_#x3b1 mutant did not overcome gemfibrozil mediated inhibition of iNOS gene expression following transient transfection of astroglial cells
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	AP-1	1.0	studies indicated that gemfibrozil suppressed cytokine induction of NF-_amp_#x3ba B AP-1 and C/EBP-_amp_#x3b2;-dependent C EBP-_amp_#x3b2 -dependent luciferase activity following transfection into
3133	EBP	emopamil binding protein (sterol isomerase)	EBP-_amp_#x3b2	0.3	suppressed cytokine induction of NF-_amp_#x3ba B AP-1 and C/EBP-_amp_#x3b2;-dependent C EBP-_amp_#x3b2 -dependent luciferase activity following transfection into glial cells
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	We recently demonstrated that a variety of PPAR-_amp_#x3b1 agonists inhibit the production of NO as well as the
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	of NO as well as the pro-inflammatory cytokines TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 IL-12 p40 and the chemokine MCP-1 by primary mouse microglia
15531	EBNA1BP2	EBNA1 binding protein 2	p40	0.3	as well as the pro-inflammatory cytokines TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 IL-12 p40 and the chemokine MCP-1 by primary mouse microglia
10618	CCL2	chemokine (C-C motif) ligand 2	MCP-1	1.3	pro-inflammatory cytokines TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 IL-12 p40 and the chemokine MCP-1 by primary mouse microglia
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.1	the production of NO as well as the pro-inflammatory cytokines TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 IL-12 p40 and the chemokine MCP-1 by primary
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Interestingly the PPAR-_amp_#x3b1 agonist fenofibrate in combination with the retinoid X receptor agonist
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	retinoic acid suppressed microglial production of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 and IL-6 in an additive manner ( Xu et al. 2005
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.0	receptor agonist 9-cis retinoic acid suppressed microglial production of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 and IL-6 in an additive manner ( Xu et
6018	IL6	interleukin 6 (interferon, beta 2)	IL-6	1.0	additive manner in inhibiting LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 and MCP-1 expression in primary astrocytes (unpublished unpublished data
10618	CCL2	chemokine (C-C motif) ligand 2	MCP-1	1.3	in inhibiting LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 and MCP-1 expression in primary astrocytes (unpublished unpublished data
11892	TNF	tumor necrosis factor (TNF superfamily, member 2)	TNF-A	0.1	in an additive manner in inhibiting LPS induction of NO TNF-_amp_#x3b1 IL-1_amp_#x3b2 IL-6 and MCP-1 expression in primary astrocytes (unpublished unpublished
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Finally our studies suggest that PPAR-_amp_#x3b1 agonists inhibit glial activation at least in part by suppressing
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	In summary we demonstrate that PPAR-_amp_#x3b1 agonists attenuate microglia and astrocyte activation in vitro
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	These results raise the possibility that PPAR-_amp_#x3b1 agonists might have benefit as a therapy in a variety
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	The effects of PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists on glial cell activation have not been examined
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	However a recent study demonstrated the PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonist GW0742 modestly inhibited LPS induction of NO production
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	This suggests that like PPAR-_amp_#x3b3 and PPAR-_amp_#x3b1 agonists PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists may suppress chronic
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	This suggests that like PPAR-_amp_#x3b3 and PPAR-_amp_#x3b1 agonists PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists may suppress chronic glial activation
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	This suggests that like PPAR-_amp_#x3b3 and PPAR-_amp_#x3b1 agonists PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonists may suppress chronic glial activation which could protect
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPARs	1.9	Effects of PPARs on neuroinflammatory and neurodegenerative disorders
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2001) 2001 first demonstrated that the PPAR-_amp_#x3b3 agonist troglitazone inhibited the development of EAE
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2002) 2002 showed that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 inhibited T cell proliferation
5962	IL10	interleukin 10	IL-10	1.0	Additionally this agonist suppressed IFN-_amp_#x3b3 IL-10 and IL-4 production by activated lymphocytes ( Diab et al.
6014	IL4	interleukin 4	IL-4	1.0	Additionally this agonist suppressed IFN-_amp_#x3b3 IL-10 and IL-4 production by activated lymphocytes ( Diab et al. 2002
5438	IFNG	interferon, gamma	IFN-G	0.2	Additionally this agonist suppressed IFN-_amp_#x3b3 IL-10 and IL-4 production by activated lymphocytes ( Diab et
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Natarajan and Bright (2002) 2002 demonstrated that the PPAR-_amp_#x3b3 agonists 15d-PGJ 2 and ciglitazone decreased the severity of both
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2003) 2003 also demonstrated that PPAR-_amp_#x3b3 deficient heterozygous mice exhibit more severe EAE than wild-type mice
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	These studies cannot be performed in PPAR-_amp_#x3b3 homozygous knockout mice which die en utero suggesting that PPAR-_amp_#x3b3
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 homozygous knockout mice which die en utero suggesting that PPAR-_amp_#x3b3 plays a critical role in development which cannot be compensated
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Future studies utilizing inducible promoters to knock out PPAR-_amp_#x3b3 in adult mice are needed to confirm the role of
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2005) 2005 demonstrated that PPAR-_amp_#x3b3 antagonists exacerbate EAE
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Collectively these studies suggest that PPAR-_amp_#x3b3 plays an important role in modulating the development of EAE
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Interestingly this suggests that PPAR-_amp_#x3b3 and RXR ligands could act cooperatively in the treatment of
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	of MS A small clinical study supports the idea that PPAR-_amp_#x3b3 agonists may be effective in the treatment of MS (
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	clinical trials are needed to assess the therapeutic potential of PPAR-_amp_#x3b3 agonists for the treatment of MS
15531	EBNA1BP2	EBNA1 binding protein 2	p40	0.3	EAE and MS We demonstrated that 15d-PGJ 2 suppresses IL-12 p40 production in both the mouse N9 microglial cell line and
11919	CD40	CD40 molecule, TNF receptor superfamily member 5	CD40	0.6	cells (APCs) APCs including microglia can produce co-stimulatory molecules including CD40 CD80 and CD86
1700	CD80	CD80 molecule	CD80	0.3	(APCs) APCs including microglia can produce co-stimulatory molecules including CD40 CD80 and CD86
1705	CD86	CD86 molecule	CD86	0.3	(APCs) APCs including microglia can produce co-stimulatory molecules including CD40 CD80 and CD86
1705	CD86	CD86 molecule	CD86	0.3	including microglia can produce co-stimulatory molecules including CD40 CD80 and CD86
1678	CD4	CD4 molecule	CD4	0.3	cognate receptors plays a critical role in the differentiation of CD4 T cells which influence the development of EAE and MS
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	the development of EAE and MS We demonstrated that the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 selectively inhibits microglial expression of CD40 but
11919	CD40	CD40 molecule, TNF receptor superfamily member 5	CD40	0.6	the PPAR-_amp_#x3b3 agonist 15d-PGJ 2 selectively inhibits microglial expression of CD40 but not CD80 and CD86 co-stimulatory molecules
1700	CD80	CD80 molecule	CD80	0.3	15d-PGJ 2 selectively inhibits microglial expression of CD40 but not CD80 and CD86 co-stimulatory molecules
1705	CD86	CD86 molecule	CD86	0.3	15d-PGJ 2 selectively inhibits microglial expression of CD40 but not CD80 and CD86 co-stimulatory molecules
1705	CD86	CD86 molecule	CD86	0.3	selectively inhibits microglial expression of CD40 but not CD80 and CD86 co-stimulatory molecules
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	This suggests that PPAR-_amp_#x3b3 agonists may modulate EAE in part by affecting microglia-T cell
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The studies outlined above suggest that PPAR-_amp_#x3b3 agonists may inhibit EAE at least in part by blocking
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	an important role in initiating EAE and MS In fact PPAR-_amp_#x3b3 agonists likely modulate the development of these disorders by a
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	PPAR-_amp_#x3b1
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	The role of PPAR-_amp_#x3b1 agonists in MS has not been thoroughly investigated
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	We demonstrated that the PPAR-_amp_#x3b1 agonists gemfibrozil and fenofibrate inhibit the clinical signs of EAE
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	In fact PPAR-_amp_#x3b1 agonists in combination with the RXR agonist 9-cis RA act
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	(2005) 2005 demonstrated that the PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 agonist GW0742 suppressed the development of EAE
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	In addition to effects on EAE PPAR agonists have been demonstrated to be effective in the treatment
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	For example PPAR-_amp_#x3b3 agonists were demonstrated to improve clinical outcomes in animal models
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	(2000) 2000 demonstrated that Tg2576 mice fed the PPAR-_amp_#x3b3 agonist ibuprofen for 6 months beginning at an age of
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	6 months beginning at an age of 10 months when amyloid plaques first develop exhibited decreased glial activation amyloid deposition and
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	amyloid	1.0	months when amyloid plaques first develop exhibited decreased glial activation amyloid deposition and dystrophic neuritis relative to untreated animals
620	APP	amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)	APP	0.3	In addition these studies demonstrated that ibuprofen altered APP processing resulting in decreased production of A_amp_#x3b2 42 in vitro
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The role of PPAR-_amp_#x3b3 agonists in modulating the development of AD was further supported
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Collectively these studies suggest that PPAR-_amp_#x3b3 agonists may be effective in the treatment of AD
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	dramatically inhibited glial activation in these studies suggesting that this PPAR-_amp_#x3b3 agonist may protect tyrosine hydroxylase positive neurons by controlling glial
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	Recent reports demonstrate that the PPAR-_amp_#x3b3 agonist pioglitazone protected motor neurons improved motor performance and extended
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	The effects of PPAR agonists on stroke have recently been investigated
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	The PPAR-_amp_#x3b3 agonists troglitazone and pioglitazone reduced infarct volume and improved neurological
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	infarct volume was reduced and neurological function was improved by PPAR-_amp_#x3b3 agonist treatment when measured 22 days after the ischemic event
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	This suggests that PPAR-_amp_#x3b3 agonists may be therapeutic in humans following stroke
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	This suggests that PPAR-_amp_#x3b3 agonists may modulate events that occur following reperfusion
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 agonists reduced CNS inflammation including macrophage/microglial macrophage microglial activation following
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	The PPAR-_amp_#x3b1 agonist fenofibrate reduced the susceptibility of apolipoprotein-E deficient mice to
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	Interestingly PPAR-_amp_#x3b1 knockout mice were not protected by fenofibrate supporting a role
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	mice were not protected by fenofibrate supporting a role for PPAR-_amp_#x3b1 in modulating pathologic events following ischemia
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	Finally the effects of PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 in modulating ischemia have recently been studied ( Arsenijevic
9235	PPARD	peroxisome proliferator-activated receptor delta	PPAR-B	1.9	In these studies PPAR-_amp_#x3b2;/_amp_#x3b4; PPAR-_amp_#x3b2 _amp_#x3b4 knockout mice demonstrated increased infarct size and increased CNS
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	PPAR agonists inhibit glial cell activation which may protect neuronal cells
9236	PPARG	peroxisome proliferator-activated receptor gamma	PPAR-G	1.9	PPAR-_amp_#x3b3 agonists of the thiazolidinedione class are currently prescribed for the
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR-A	1.9	currently prescribed for the treatment of type II diabetes while PPAR-_amp_#x3b1 agonists including fibrates are commonly prescribed for hypertriglyceridemia
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	should facilitate future clinical trials evaluating the efficacy of these PPAR agonists in the treatment of these human disorders of the
9232	PPARA	peroxisome proliferator-activated receptor alpha	PPAR	1.9	Finally understanding the molecular mechanisms by which PPAR agonists regulate CNS inflammation will also be critical in developing
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	ap 1	1.0	for example these agonists inhibit transcription factors including nf _amp_#x3ba;b ap 1 and stat 1 from activating gene expression in this manner.
10618	CCL2	chemokine (C-C motif) ligand 2	mcp 1	1.0	zolidinediones which are commonly used to treat type ii diabetes and the naturally occurring 15d pgj 2 inhibited no as well as the cytokines il 1_amp_#x3b2; il 6 and tnf _amp_#x3b1; and the chemokine mcp 1 by both primary mouse microglia and astrocytes storer et al. 2005a and storer et al. 2005b .
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	recently we demonstrated that thiazolidinediones which are commonly used to treat type ii diabetes and the naturally occurring 15d pgj 2 inhibited no as well as the cytokines il 1_amp_#x3b2; il 6 and tnf _amp_#x3b1; and the chemokine mcp 1 by both primary mouse microglia and astrocytes storer et al. 2005a and storer et al. 2005b .
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	2004 demonstrated that the ppar _amp_#x3b3; agonist 15d pgj 2 inhibited lps induction of no tnf _amp_#x3b1; il 1_amp_#x3b2; and il 6 in primary astrocytes.
8975	PIK3CA	phosphoinositide-3-kinase, catalytic, alpha polypeptide	phosphatidylinositol 3 kinase	1.0	furthermore the studies demonstrated that 15d pgj 2 also altered astrocyte expression of these pro inflammatory molecules by inhibiting the phosphatidylinositol 3 kinase akt signaling pathway.
11364	STAT3	signal transducer and activator of transcription 3 (acute-phase response factor)	stat3	1.0	2003 demonstrated that the ppar _amp_#x3b3; agonists 15d pgj 2 and rosiglitazone inhibit the phosphorylation of stat1 stat3 jak1 and jak2 in microglia and astrocytes.
19383	SOCS1	suppressor of cytokine signaling 1	socs 1	1.0	the authors further demonstrated that these agonists induce the expression of suppressor of cytokine signaling socs 1 and 3 which alters jak/stat phosphorylation and jak/stat mediated signaling.
1984	CISH	cytokine inducible SH2-containing protein	suppressor of cytokine signaling	1.0	the authors further demonstrated that these agonists induce the expression of suppressor of cytokine signaling socs 1 and 3 which alters jak/stat phosphorylation and jak/stat mediated signaling.
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	for example these ppar _amp_#x3b3; agonists blocked tnf _amp_#x3b1; and il 6 expression by monocytes.
9605	PTGS2	prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)	cox 2	1.0	recent studies demonstrated that tzds block the production of inos tnf _amp_#x3b1; il 6 and cox 2 by primary rat microglia and astrocytes and protected cortical neurons in a neuron glia co culture paradigm.
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	recent studies demonstrated that tzds block the production of inos tnf _amp_#x3b1; il 6 and cox 2 by primary rat microglia and astrocytes and protected cortical neurons in a neuron glia co culture paradigm.
3796	FOS	v-fos FBJ murine osteosarcoma viral oncogene homolog	ap 1	1.0	furthermore these studies indicated that gemfibrozil suppressed cytokine induction of nf _amp_#x3ba;b ap 1 and c/ebp _amp_#x3b2; dependent luciferase activity following transfection into glial cells.
10618	CCL2	chemokine (C-C motif) ligand 2	mcp 1	1.0	cently demonstrated that a variety of ppar _amp_#x3b1; agonists inhibit the production of no as well as the pro inflammatory cytokines tnf _amp_#x3b1; il 1_amp_#x3b2; il 6 il 12 p40 and the chemokine mcp 1 by primary mouse microglia.
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	we recently demonstrated that a variety of ppar _amp_#x3b1; agonists inhibit the production of no as well as the pro inflammatory cytokines tnf _amp_#x3b1; il 1_amp_#x3b2; il 6 il 12 p40 and the chemokine mcp 1 by primary mouse microglia.
10477	RXRA	retinoid X receptor, alpha	retinoid x receptor	1.0	interestingly the ppar _amp_#x3b1; agonist fenofibrate in combination with the retinoid x receptor agonist 9 cis retinoic acid suppressed microglial production of no tnf _amp_#x3b1; il 1_amp_#x3b2; and il 6 in an additive manner xu et al. 2005 .
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	terestingly the ppar _amp_#x3b1; agonist fenofibrate in combination with the retinoid x receptor agonist 9 cis retinoic acid suppressed microglial production of no tnf _amp_#x3b1; il 1_amp_#x3b2; and il 6 in an additive manner xu et al. 2005 .
10618	CCL2	chemokine (C-C motif) ligand 2	mcp 1	1.0	similarly fenofibrate and 9 cis ra acted in an additive manner in inhibiting lps induction of no tnf _amp_#x3b1; il 1_amp_#x3b2; il 6 and mcp 1 expression in primary astrocytes unpublished data .
6018	IL6	interleukin 6 (interferon, beta 2)	il 6	1.0	similarly fenofibrate and 9 cis ra acted in an additive manner in inhibiting lps induction of no tnf _amp_#x3b1; il 1_amp_#x3b2; il 6 and mcp 1 expression in primary astrocytes unpublished data .
6925	MBP	myelin basic protein	myelin basic protein	1.0	using neural antigen specific t cells from the spleen of myelin basic protein ac 1_amp_#x2013;11 tcr transgenic mice which when activated with antigen can induce eae diab et al.
5962	IL10	interleukin 10	il 10	1.0	additionally this agonist suppressed ifn _amp_#x3b3; il 10 and il 4 production by activated lymphocytes diab et al. 2002 .
6014	IL4	interleukin 4	il 4	1.0	additionally this agonist suppressed ifn _amp_#x3b3; il 10 and il 4 production by activated lymphocytes diab et al. 2002 .
11782	TH	tyrosine hydroxylase	tyrosine hydroxylase	1.0	this disease is characterized by death of tyrosine hydroxylase positive neurons in the striatum and substantia nigra.
11782	TH	tyrosine hydroxylase	tyrosine hydroxylase	1.0	pioglitazone dramatically inhibited glial activation in these studies suggesting that this ppar _amp_#x3b3; agonist may protect tyrosine hydroxylase positive neurons by controlling glial activation breidert et al. 2002 and dehmer et al. 2004 .
11179	SOD1	superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))	superoxide dismutase 1	1.0	recent reports demonstrate that the ppar _amp_#x3b3; agonist pioglitazone protected motor neurons improved motor performance and extended the survival of superoxide dismutase 1 g93a transgenic mice an animal model of als.
19383	SOCS1	suppressor of cytokine signaling 1	suppressor of cytokine signaling 1	1.0	finally these studies demonstrated reduced gliosis decreased nf _amp_#x3ba;b and increased suppressor of cytokine signaling 1 and 3 expression in pioglitazone treated animals kiaei et al. 2005 and sch_amp_#xfc;tz et al. 2005 .
613	APOE	apolipoprotein E	apolipoprotein e	1.0	the ppar _amp_#x3b1; agonist fenofibrate reduced the susceptibility of apolipoprotein e deficient mice to stroke.