Crosstalk between SDF-1/CXCR4 and SDF-1/CXCR7 in cardiac stem cell migration

被引：70

作者：

Chen, Dong ^{[1
]}

Xia, Yanli ^{[1
]}

Zuo, Ke ^{[1
]}

Wang, Ying ^{[1
]}

Zhang, Shiying ^{[1
]}

Kuang, Dong ^{[1
]}

Duan, Yaqi ^{[1
]}

Zhao, Xia ^{[1
]}

Wang, Guoping ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Inst Pathol, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China

来源：

SCIENTIFIC REPORTS | 2015年 / 5卷

基金：

中国国家自然科学基金;

关键词：

CHEMOKINE RECEPTOR CXCR7; GENOME-WIDE ASSOCIATION; MYOCARDIAL-INFARCTION; BETA-ARRESTIN; UP-REGULATION; FACTOR-I; RAF; FACTOR-1-ALPHA; ACTIVATION; CXCL12;

D O I：

10.1038/srep16813

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

Stromal cell-derived factor 1 (SDF-1) is a chemokine that can be expressed in injured cardiomyocytes after myocardial infarction (MI). By combining with its receptor CXCR4, SDF-1 induced stem and progenitor cells migration. CXCR7, a novel receptor for SDF-1, has been identified recently. We aimed to explore the roles of SDF-1/CXCR4 and SDF-1/CXCR7 pathway and their crosstalk in CSCs migration. In the present study, CXCR4 and CXCR7 expression were identified in CSCs. Transwell assay showed that SDF-1 caused CSCs migration in a dose-and time-dependent manner, which could be significantly suppressed by CXCR4 or CXCR7 siRNA. Phospho-ERK, phospho-Akt and Raf-1 significantly elevated in CSCs with SDF-1 stimulation. Knockdown of CXCR4 or CXCR7 significantly decreased phospho-ERK or phospho-Akt, respectively, and eventually resulted in the inhibition of CSCs migration. Moreover, western blot showed that MK2206 (Akt inhibitor) increased the expression of phospho-ERK and Raf-1, whereas PD98059 (ERK inhibitor) had no effect on phospho-Akt and Raf-1. GW5074 (Raf-1 inhibitor) upregulated the expression of phospho-ERK, but had no effect on phospho-Akt. The present study indicated that SDF-1/CXCR7/Akt and SDF-1/CXCR4/ERK pathway played important roles in CSCs migration. Akt phosphorylation inhibited Raf-1 activity, which in turn dephosphorylated ERK and negatively regulated CSCs migration.

引用

页数：9

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