Catestatin enhances ATP-induced activation of glial cells mediated by purinergic receptor P2X4.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Errong Du, Anhui Wang, Rongping Fan, Lilou Rong, Runan Yang, Juping Xing, Xiangchao Shi, Bao Qiao, Ruoyang Yu, Changshui Xu
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引用次数: 2

Abstract

The activation of glial cells and its possible mechanism play an extremely important role in understanding the pathophysiological process of some clinical diseases, and catestatin (CST) is involved in regulating this activation. In this project, we found that CST could enhance the activation of satellite glial cells (SGCs) and microglial cells and that the expression of P2X4 was increased; the co-expression of the P2X4 receptor with glial fibrillary acidic protein (GFAP) and the P2X4 receptor with CD11b was also increased significantly in glial cells of the ATP + CST group, and TNF-α and IL-1β also showed a rising trend; the expression of phosphorylated ERK1/2 was also increased in the ATP + CST group. In summary, we conclude that CST could enhance ATP-induced activation of SGCs and microglial cells mediated by the P2X4 receptor and that the ERK1/2 signaling pathway may be involved in this activation process.

Catestatin增强嘌呤能受体P2X4介导的atp诱导的胶质细胞活化。
神经胶质细胞的活化及其可能的机制在了解一些临床疾病的病理生理过程中起着极其重要的作用,而catestatin (CST)参与调节这种活化。在本项目中,我们发现CST可以增强卫星胶质细胞(SGCs)和小胶质细胞的活化,并增加P2X4的表达;ATP + CST组胶质细胞中P2X4受体与胶质原纤维酸性蛋白(GFAP)和P2X4受体与CD11b的共表达也显著增加,TNF-α和IL-1β也呈上升趋势;ATP + CST组磷酸化ERK1/2的表达也增加。综上所述,我们得出结论,CST可以增强atp诱导的P2X4受体介导的SGCs和小胶质细胞的激活,并且ERK1/2信号通路可能参与了这一激活过程。
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来源期刊
Journal of Receptors and Signal Transduction
Journal of Receptors and Signal Transduction 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.
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