• Wenbin Li, Fan Yang, Jinxing Gao, Yushi Tang, Jing Wang, and Yujun Pan.
• Department of Neurology, First Clinical College of Harbin Medical University, Room 501, Building 3, 23 Youzheng Street, Harbin, Heilongjiang Province, 150001, People's Republic of China.
• Neuroscience. 2019 Sep 1; 415: 147160147-160.

AbstractStroke is a major life-threatening and disabling disease with a restricted therapeutic approach. Bone marrow stromal cells (BMSCs) possess proliferative ability and a multi-directional differentiation potential, and secrete a range of trophic/growth factors that can protect neurons after cerebral ischemia/reperfusion. Transient receptor potential canonical (TRPC) is a family of non-selective channels permeable to Ca2+, with several functions including neuronal survival. Over-expression of TRPC6, a subtype of the TRPC family, was shown to protect neurons against cerebral ischemia/reperfusion injury. However, it remains unclear whether over-expression of TRPC6 in BMSCs can further reduce brain injury after ischemia/reperfusion. In the present study, we report that over-expression of TRPC6 via a CRISPR-based synergistic activation mediator in BMSCs provided a greater reduction of brain injury in a rat model of ischemia/reperfusion. Further, the improved neurofunctional outcomes were associated with increased TRPC6 and brain derived neurotrophic factor expression levels. Overall, these data suggest that TRPC6 over-expressing BMSCs may be a promising therapeutic agent for ischemic stroke.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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