Inhibition of interleukin-1β production by extracellular acidification through the TDAG8/cAMP pathway in mouse microglia

被引：49

作者：

Jin, Ye ^{[1
]}

Sato, Koichi ^{[1
]}

Tobo, Ayaka ^{[1
]}

Mogi, Chihiro ^{[1
]}

Tobo, Masayuki ^{[1
]}

Murata, Naoya ^{[1
]}

Ishii, Satoshi ^{[2
]}

Im, Dong-Soon ^{[3
]}

Okajima, Fumikazu ^{[1
]}

机构：

[1] Gunma Univ, Inst Mol & Cellular Regulat, Lab Signal Transduct, Maebashi, Gunma 3718512, Japan

[2] Akita Univ, Grad Sch Med, Dept Immunol, Akita 010, Japan

[3] Pusan Natl Univ, Coll Pharm, Pharmacol Lab, Pusan, South Korea

来源：

JOURNAL OF NEUROCHEMISTRY | 2014年 / 129卷 / 04期

基金：

日本学术振兴会;

关键词：

acidification; cAMP; interleukin-1; microglia; protein kinase A; TDAG8; NF-KAPPA-B; PROTEIN-COUPLED RECEPTORS; TOLL-LIKE RECEPTORS; INFLAMMATORY RESPONSES; CYTOKINE PRODUCTION; CA2+ INFLUX; ACTIVATION; BRAIN; PH; IDENTIFICATION;

D O I：

10.1111/jnc.12661

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A number of studies have shown that extracellular acidification in brain is observed in ischemia and neurodegenerative disorders. However, the molecular mechanism by which extracellular acidification regulates the biological activities of microglia remains uncharacterized. Here, we examined the extracellular acidic pH regulation of IL-1 production, especially focusing on TDAG8, a member of OGR1 family receptors. Our results suggest that extracellular acidic pH inhibited lipopolysaccharide -induced IL-1 production at least partly through the TDAG8/cAMP pathway, by inhibiting ERK and JNK activities.

引用

页码：683 / 695

页数：13

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