Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: Implications for multiple sclerosis
Peroxisome proliferator-activated receptor (PPAR)-γ agonists, including thiazolidinediones (TZDs) and 15-deoxy-Δ 12,14 prostaglandin J 2 (15d-PGJ 2), have been shown to be effective in the treatment of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). This...
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| Veröffentlicht in: | Journal of neuroimmunology 2005-04, Vol.161 (1), p.113-122 |
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| creator | Storer, Paul D. Xu, Jihong Chavis, Janet Drew, Paul D. |
| description | Peroxisome proliferator-activated receptor (PPAR)-γ agonists, including thiazolidinediones (TZDs) and 15-deoxy-Δ
12,14 prostaglandin J
2 (15d-PGJ
2), have been shown to be effective in the treatment of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). This study aimed to compare the anti-inflammatory actions of three TZDs – rosiglitazone, pioglitazone, and ciglitazone – with those of 15d-PGJ
2 on stimulated mouse microglia and astrocytes. The results show that TZDs and 15d-PGJ
2 are effective in inhibiting production of nitric oxide, the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, and the chemokine MCP-1 from microglia and astrocytes. However, 15d-PGJ
2 was a more potent suppressor of pro-inflammatory activity than the TZDs. These studies suggest that PPAR-γ agonists modulate EAE, at least in part, by inhibiting the activation of microglia and astrocytes. The studies further suggest that PPAR-γ agonists may be effective in the treatment of MS. |
| doi_str_mv | 10.1016/j.jneuroim.2004.12.015 |
| format | Article |
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12,14 prostaglandin J
2 (15d-PGJ
2), have been shown to be effective in the treatment of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). This study aimed to compare the anti-inflammatory actions of three TZDs – rosiglitazone, pioglitazone, and ciglitazone – with those of 15d-PGJ
2 on stimulated mouse microglia and astrocytes. The results show that TZDs and 15d-PGJ
2 are effective in inhibiting production of nitric oxide, the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, and the chemokine MCP-1 from microglia and astrocytes. However, 15d-PGJ
2 was a more potent suppressor of pro-inflammatory activity than the TZDs. These studies suggest that PPAR-γ agonists modulate EAE, at least in part, by inhibiting the activation of microglia and astrocytes. The studies further suggest that PPAR-γ agonists may be effective in the treatment of MS.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2004.12.015</identifier><identifier>PMID: 15748950</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>15d-PGJ 2 ; Animals ; Animals, Newborn ; Astrocytes - drug effects ; Astrocytes - physiology ; Blotting, Western - methods ; Cell Survival - drug effects ; Cells, Cultured ; Cerebral Cortex - cytology ; Chemokine ; Chemokines - secretion ; Cytokine ; Cytokines - pharmacology ; Cytokines - secretion ; Dose-Response Relationship, Drug ; Drug Interactions ; Enzyme-Linked Immunosorbent Assay - methods ; Gene Expression Regulation - drug effects ; Glia ; Inhibitory Concentration 50 ; Lipopolysaccharides - pharmacology ; Mice ; Microglia - drug effects ; Microglia - physiology ; Nitric Oxide - metabolism ; PPAR ; PPAR gamma - agonists ; Prostaglandin D2 - analogs & derivatives ; Prostaglandin D2 - pharmacology ; Thiazolidinedione ; Thiazolidinediones - pharmacology</subject><ispartof>Journal of neuroimmunology, 2005-04, Vol.161 (1), p.113-122</ispartof><rights>2005 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-8dc4fc9d699ca70ebe756592bf848d6b59256de3c274608b0d30a7948c7f6a853</citedby><cites>FETCH-LOGICAL-c494t-8dc4fc9d699ca70ebe756592bf848d6b59256de3c274608b0d30a7948c7f6a853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jneuroim.2004.12.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15748950$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Storer, Paul D.</creatorcontrib><creatorcontrib>Xu, Jihong</creatorcontrib><creatorcontrib>Chavis, Janet</creatorcontrib><creatorcontrib>Drew, Paul D.</creatorcontrib><title>Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: Implications for multiple sclerosis</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>Peroxisome proliferator-activated receptor (PPAR)-γ agonists, including thiazolidinediones (TZDs) and 15-deoxy-Δ
12,14 prostaglandin J
2 (15d-PGJ
2), have been shown to be effective in the treatment of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). This study aimed to compare the anti-inflammatory actions of three TZDs – rosiglitazone, pioglitazone, and ciglitazone – with those of 15d-PGJ
2 on stimulated mouse microglia and astrocytes. The results show that TZDs and 15d-PGJ
2 are effective in inhibiting production of nitric oxide, the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, and the chemokine MCP-1 from microglia and astrocytes. However, 15d-PGJ
2 was a more potent suppressor of pro-inflammatory activity than the TZDs. These studies suggest that PPAR-γ agonists modulate EAE, at least in part, by inhibiting the activation of microglia and astrocytes. The studies further suggest that PPAR-γ agonists may be effective in the treatment of MS.</description><subject>15d-PGJ 2</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - physiology</subject><subject>Blotting, Western - methods</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Chemokine</subject><subject>Chemokines - secretion</subject><subject>Cytokine</subject><subject>Cytokines - pharmacology</subject><subject>Cytokines - secretion</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>Enzyme-Linked Immunosorbent Assay - methods</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glia</subject><subject>Inhibitory Concentration 50</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Mice</subject><subject>Microglia - drug effects</subject><subject>Microglia - physiology</subject><subject>Nitric Oxide - metabolism</subject><subject>PPAR</subject><subject>PPAR gamma - agonists</subject><subject>Prostaglandin D2 - analogs & derivatives</subject><subject>Prostaglandin D2 - pharmacology</subject><subject>Thiazolidinedione</subject><subject>Thiazolidinediones - pharmacology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFvFCEUx4nR2HX1KzScvM0UGBgYT5pGbZMmetAzYeDNls0wjMA27cfwG8u6azz29MjLD97780PokpKWEtpf7dv9AocUfWgZIbylrCVUvEAbqiRrFGf0JdpUUDRCMnWB3uS8J5Xo-PAaXVAhuRoE2aDf3yHFR59jALymOPsJkikxNcYW_2AKOJzAwnps7UwIBptdXHwuGfvl3o--4HIP-Ez7uOA44eBtirvZV3hx2OSSon0qkD_g27DO3v4FM55iwuEwF7_OgLOd6ybZ57fo1WTmDO_OdYt-fvn84_qmufv29fb6011j-cBLo5zlkx1cPwzWSAIjSNGLgY2T4sr1Yz2K3kFnmeQ9USNxHTFy4MrKqTdKdFv0_vRujf3rALno4LOFeTYLxEPWjEg6ENk9C1LZCcZ6WcH-BNb0OSeY9Jp8MOlJU6KP1vRe_7Omj9Y0ZfroZIsuzxMOYwD3_9pZUwU-ngCoH_LgIelsPSwWnK92inbRPzfjD2bssSA</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Storer, Paul D.</creator><creator>Xu, Jihong</creator><creator>Chavis, Janet</creator><creator>Drew, Paul D.</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope></search><sort><creationdate>20050401</creationdate><title>Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: Implications for multiple sclerosis</title><author>Storer, Paul D. ; Xu, Jihong ; Chavis, Janet ; Drew, Paul D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-8dc4fc9d699ca70ebe756592bf848d6b59256de3c274608b0d30a7948c7f6a853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>15d-PGJ 2</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - physiology</topic><topic>Blotting, Western - methods</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Chemokine</topic><topic>Chemokines - secretion</topic><topic>Cytokine</topic><topic>Cytokines - pharmacology</topic><topic>Cytokines - secretion</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>Enzyme-Linked Immunosorbent Assay - methods</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glia</topic><topic>Inhibitory Concentration 50</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Mice</topic><topic>Microglia - drug effects</topic><topic>Microglia - physiology</topic><topic>Nitric Oxide - metabolism</topic><topic>PPAR</topic><topic>PPAR gamma - agonists</topic><topic>Prostaglandin D2 - analogs & derivatives</topic><topic>Prostaglandin D2 - pharmacology</topic><topic>Thiazolidinedione</topic><topic>Thiazolidinediones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Storer, Paul D.</creatorcontrib><creatorcontrib>Xu, Jihong</creatorcontrib><creatorcontrib>Chavis, Janet</creatorcontrib><creatorcontrib>Drew, Paul D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Storer, Paul D.</au><au>Xu, Jihong</au><au>Chavis, Janet</au><au>Drew, Paul D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: Implications for multiple sclerosis</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>161</volume><issue>1</issue><spage>113</spage><epage>122</epage><pages>113-122</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Peroxisome proliferator-activated receptor (PPAR)-γ agonists, including thiazolidinediones (TZDs) and 15-deoxy-Δ
12,14 prostaglandin J
2 (15d-PGJ
2), have been shown to be effective in the treatment of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). This study aimed to compare the anti-inflammatory actions of three TZDs – rosiglitazone, pioglitazone, and ciglitazone – with those of 15d-PGJ
2 on stimulated mouse microglia and astrocytes. The results show that TZDs and 15d-PGJ
2 are effective in inhibiting production of nitric oxide, the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, and the chemokine MCP-1 from microglia and astrocytes. However, 15d-PGJ
2 was a more potent suppressor of pro-inflammatory activity than the TZDs. These studies suggest that PPAR-γ agonists modulate EAE, at least in part, by inhibiting the activation of microglia and astrocytes. The studies further suggest that PPAR-γ agonists may be effective in the treatment of MS.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>15748950</pmid><doi>10.1016/j.jneuroim.2004.12.015</doi><tpages>10</tpages></addata></record> |
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| subjects | 15d-PGJ 2 Animals Animals, Newborn Astrocytes - drug effects Astrocytes - physiology Blotting, Western - methods Cell Survival - drug effects Cells, Cultured Cerebral Cortex - cytology Chemokine Chemokines - secretion Cytokine Cytokines - pharmacology Cytokines - secretion Dose-Response Relationship, Drug Drug Interactions Enzyme-Linked Immunosorbent Assay - methods Gene Expression Regulation - drug effects Glia Inhibitory Concentration 50 Lipopolysaccharides - pharmacology Mice Microglia - drug effects Microglia - physiology Nitric Oxide - metabolism PPAR PPAR gamma - agonists Prostaglandin D2 - analogs & derivatives Prostaglandin D2 - pharmacology Thiazolidinedione Thiazolidinediones - pharmacology |
| title | Peroxisome proliferator-activated receptor-gamma agonists inhibit the activation of microglia and astrocytes: Implications for multiple sclerosis |
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