Biochem Biophys Res Commun. 2018 Sep 18;503(4):2993-2997. doi: 10.1016/j.bbrc.2018.08.083. Epub 2018 Aug 14.
Bao M1, Liu S2, Yu XY3, Wu C1, Chen Q1, Ding H1, Shen C1, Wang B1, Wang S1, Song YH4, Li Y5.
Author Information
1Cyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, China.
2Suzhou Vocational Health College, Suzhou Key Laboratory of Biotechnology for Laboratory Medicine, Suzhou, 215009, Jiangsu Province, China.
3Key Laboratory of Molecular Clinical Pharmacology and Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
4Cyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, Soochow University, Suzhou, China. Electronic address: yaohua_song1@yahoo.com.
5Department of Cardiovascular Surgery, The First Affiliated Hospital and The Institute for Cardiovascular Science, Soochow University, Suzhou, Jiangsu, 215123, China. Electronic address: yangxin_li@yahoo.com.
Abstract
RUNX1 is a transcription factor that is not expressed in uninjured muscles, but can be detected in denervated muscles, suggesting a role of RUNX1 in muscle's response to injury. However, the role of RUNX1 in muscle's response to ischemia has not been reported. Our study showed that Runx1 is up regulated in skeletal muscle during ischemia reperfusion induced injury. Over-expression of Runx1 in C2C12?cells inhibits myogenic differentiation, but promotes proliferation of myoblasts. Consistent with these findings, we found that Runx1 expression was decreased in differentiated satellite cells. Our results indicate that Runx1 regulates muscle regeneration by promoting proliferation of satellite cells.