RT期刊文章SR电子T1雪旺细胞表达肾上腺受体亚型:激活的ACTH 1-39和Alpha-MSH增强扩散(P1.430)摩根富林明神经病学神经学乔FD Lippincott Williams &威尔金斯SP P1.430 VO 90 15 A1罗伯特补充Lisak A1贝弗利Bealmear A1 Liljana Nedle首页koska A1乔伊斯本杰明一起珍藏的东西年2018 UL //www.ez-admanager.com/content/90/15_Supplement/P1.430.abstract AB目的:调查ex-pression肾上腺受体(MCR)亚型的雪旺细胞(SC)和是否MCR调节SC扩散。背景:ACTH1-39信号通过mcr增加环腺苷酸,SC增殖和分化的重要调节器。老鼠少突神经胶质(OL)和他们的祖细胞(OPC)表达MCR亚型受体,M3R中的,MC5R。MCR受体激动剂ACTH1-39保护OL和OPC体外机制导致多发性硬化症损害引起的死亡(2014年本杰明一起珍藏的东西et al . 2013年);保护是模仿MCR受体激动剂和被MCR拮抗剂(本杰明一起珍藏的东西et al . 2017年)。mcr的激活也刺激OPC扩散。表达式和函数SC MCR亚型的不清楚。设计/方法:文化丰富了SC(> 97%)准备从新生大鼠坐骨神经(Lisak et al . 1991年)。表面MCR ex-pression被评估使用MCR亚型抗体免疫细胞化学,与特定的阻断肽作为控制。SC ACTH1-39对待,alpha-MSH或NDP-MSH。扩散被溴脱氧尿苷公司评估。 MCR subtype specific agonists and antagonists were tested for their effects on ACTH-stimulated proliferation.Results: SC express MC1R, MC3R, MC4R and MC5R, and no MC2R, as expected given its expression is localized to the adrenals. Both ACTH and alpha-MSH stimulated proliferation. Five days after addition of 200 nM ACTH1-39, SC proliferation was 9.2% compared to 3.0% in control cultures. Similarly, alpha-MSH and NDP-MSH increased proliferation to 7.5% and 6.2%, respectively. These proliferative effects are mimicked by MCR subtype specific agonists. MC3R antagonist PG106 and MC4R antagonist HS024 blocked the ACTH-induced proliferation.Conclusions: SC express surface MC1R, MC3R, MC4R and MC5R. Increased SC proliferation in response to ACTH1-39 and MCR agonists indicates that MCRs on SC are functional and activate signaling pathways that stimulate proliferation. Increased SC proliferation is an important regenerative response in traumatic and demyelinating neuropathies, including those of inflammatory, inherited/degenerative, toxic and metabolic origin.Study Supported by: Parker Webber Chair in Neurology Endowment (DMC Foundation/Wayne State University).Disclosure: Dr. Lisak has received personal compensation for activities compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Teva Neuroscience, Teva Pharmaceuticals, Ltd, GLG Consultants, Syntimmune, Celgene, Alexion, Alpha Sites, Insights Consulting, and Alexion. Dr. Lisak has received research support from NMSS, NIH, Teva Pharmaceuticals, Novartis, Genetec (Roche), MedImmune, and Chugai. Dr. Bealmear has nothing to disclose. Dr. Nedelkoska has nothing to disclose. Dr. Benjamins has nothing to disclose.