Accelerated degradation of retinoic acid by activated microglia

被引：30

作者：

Hellmann-Regen, Julian ^{[1
,2
,3
]}

Kronenberg, Golo ^{[1
,2
,4
]}

Uhlemann, Ria ^{[1
,2
]}

Freyer, Dorette ^{[2
]}

Endres, Matthias ^{[1
,2
,5
]}

Gertz, Karen ^{[1
,2
]}

机构：

[1] Charite, Ctr Stroke Res Berlin, D-10117 Berlin, Germany

[2] Charite, Klin & Poliklin Neurol, D-10117 Berlin, Germany

[3] Charite Campus Benjamin Franklin, Klin & Hsch Ambulanz Psychiat & Psychotherapie, D-14050 Berlin, Germany

[4] Charite Campus Mitte, Klin Psychiat & Psychotherapie, D-10117 Berlin, Germany

[5] Charite, Cluster Excellence NeuroCure, D-10117 Berlin, Germany

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 256卷 / 1-2期

关键词：

Microglia; LPS; Cytochrome P450 enzymes; Neuroinflammation; Retinoic acid; INHIBIT INFLAMMATORY RESPONSES; TNF-ALPHA; DEPENDENT SURVIVAL; CEREBRAL-ISCHEMIA; RECEPTOR-ALPHA; EXPRESSION; NEURONS; CELL; NEUROGENESIS; METABOLISM;

D O I：

10.1016/j.jneuroim.2012.11.005

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

In the brain, retinoic acid (RA) concentrations are under tight spatio-temporal control. Here, we show that challenge of primary mouse microglia with lipopolysaccharide (LPS) results in increased release of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha). Co-administration of RA attenuated microglial activation. Similarly, pretreatment with RA-metabolism inhibitor liarozole potently reduced NO and TNF-alpha release. Conversely, activated microglia showed increased protein expression of RA-degrading cytochromes CYP26A1, CYP26B1, CYP3A4 and CYP2C. Correspondingly, RA catabolism by activated microglia was significantly increased. Our results indicate that RA reduces microglial activation, but also, conversely, that the activation state of microglia influences RA metabolism. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：1 / 6

页数：6

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