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食欲素-A通过Ca2+依赖的蛋白激酶Cα和细胞外信号调节激酶1/2信号通路促进培养的大鼠星形胶质细胞迁移。

Orexin-A promotes cell migration in cultured rat astrocytes via Ca2+-dependent PKCα and ERK1/2 signals.

作者信息

Shu Qing, Hu Zhuang-Li, Huang Chao, Yu Xiao-Wei, Fan Hua, Yang Jing-Wen, Fang Peng, Ni Lan, Chen Jian-Guo, Wang Fang

机构信息

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China; The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, Hubei, China.

出版信息

PLoS One. 2014 Apr 18;9(4):e95259. doi: 10.1371/journal.pone.0095259. eCollection 2014.

DOI:10.1371/journal.pone.0095259
PMID:24748172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3991588/
Abstract

Orexin-A is an important neuropeptide involved in the regulation of feeding, arousal, energy consuming, and reward seeking in the body. The effects of orexin-A have widely studied in neurons but not in astrocytes. Here, we report that OX1R and OX2R are expressed in cultured rat astrocytes. Orexin-A stimulated the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), and then induced the migration of astrocytes via its receptor OX1R but not OX2R. Orexin-A-induced ERK1/2 phosphorylation and astrocytes migration are Ca2+-dependent, since they could be inhibited by either chelating the extracellular Ca2+ or blocking the pathway of store-operated calcium entry (SOCE). Furthermore, both non-selective protein kinase C (PKC) inhibitor and PKCα selective inhibitor, but not PKCδ inhibitor, prevented the increase in ERK1/2 phosphorylation and the migration of astrocytes, indicating that the Ca2+-dependent PKCα acts as the downstream of the OX1R activation and mediates the orexin-A-induced increase in ERK1/2 phosphorylation and cell migration. In conclusion, these results suggest that orexin-A can stimulate ERK1/2 phosphorylation and then facilitate the migration of astrocytes via PLC-PKCα signal pathway, providing new knowledge about the functions of the OX1R in astrocytes.

摘要

食欲素A是一种重要的神经肽，参与机体的进食、觉醒、能量消耗和奖赏寻求调节。食欲素A的作用在神经元中已得到广泛研究，但在星形胶质细胞中尚未有研究。在此，我们报道OX1R和OX2R在培养的大鼠星形胶质细胞中表达。食欲素A刺激细胞外信号调节激酶1/2（ERK1/2）的磷酸化，然后通过其受体OX1R而非OX2R诱导星形胶质细胞迁移。食欲素A诱导的ERK1/2磷酸化和星形胶质细胞迁移是Ca2+依赖性的，因为它们可通过螯合细胞外Ca2+或阻断储存性钙内流（SOCE）途径而受到抑制。此外，非选择性蛋白激酶C（PKC）抑制剂和PKCα选择性抑制剂而非PKCδ抑制剂可阻止ERK1/2磷酸化增加和星形胶质细胞迁移，表明Ca²⁺依赖性PKCα作为OX1R激活的下游，介导食欲素A诱导的ERK1/2磷酸化增加和细胞迁移。总之，这些结果表明食欲素A可刺激ERK1/2磷酸化，然后通过PLC-PKCα信号通路促进星形胶质细胞迁移，为OX1R在星形胶质细胞中的功能提供了新知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d4/3991588/82664cd5d251/pone.0095259.g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d4/3991588/2138b6d5f168/pone.0095259.g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d4/3991588/82664cd5d251/pone.0095259.g008.jpg

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