Proteinase-activated receptor 2 modulates corticotropin releasing hormone-induced brain-derived neurotrophic factor release from microglial cells.
作者： Yongzhi Fan , Jingli Chen , Jun Ye , Hong Yan , Yi Cai
DOI: 10.1002/CBIN.10185
关键词: Apoptosis 、 Internal medicine 、 Microglia 、 Endocrinology 、 Corticotropin-releasing hormone 、 Protease-activated receptor 2 、 Tryptase 、 Brain-derived neurotrophic factor 、 Receptor 、 Chemistry 、 Neurotrophic factors
摘要: Brain-derived neurotrophic factor (BDNF) plays a critical role in the pathogenesis of neuropathic pain, but its regulation BDNF release is not fully understood. To further understand release, microglial cell line, C8-D1A (microglia, short), were cultured as model. The levels determined by enzyme-linked immunoassay. Apoptotic microglia assessed flow cytometry. protease-activated receptor 2 (PAR2) was activated tryptase. Exposure to corticotripin releasing hormone (CRH) induced from microglia. Apoptosis evident after activation CRH. Tryptase-induced PAR2 reduced frequency apoptosis microglia, enhanced culture medium, which partially blocked antagonists. We conclude that agonists can promote microglia; antagonists may be potential therapeutic target attenuate BDNF-related pain.
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