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Effect of Overexpression CXCR4/CXCR7 on Proliferation， Migration，Anti-oxidative Stress Damage of Mouse Embryonic Liver Stem Cell
Xiao Cheng1, Luo Qing2, Kang Quan1*, Yang Bo1, Wang Jian1, Gong Mengjia2, Bi Yang2
1Department of Hepatology, Children’s Hospital of Chongqing Medical University, Chongqing 400014, China;
2Laboratory of Stem Cell Biology and Therapy, Children’s Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing 400014, China
2Laboratory of Stem Cell Biology and Therapy, Children’s Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing 400014, China
Abstract: The aim of this artical is to investigate the effect of SDF-1 (stromal cell-derived factor-1)/CXCR4 (chemotaxis cytokine receptor 4) and SDF-1/CXCR7 on the proliferation， migration and anti-oxidative stress of mouse embryonic liver stem cells. Recombinant adenovirus which containing CXCR4 or CXCR7 gene was applied to infect HP14-19， respectively. Flow cytometry and Western blot were used to detect the expression of CXCR4 or CXCR7 as membrane receptors. Cell proliferation activity was detected by MTT assay. Transwell assay was carried out to evaluate the SDF-1 induced migration ability of HP14-19 with CXCR4 or CXCR7 overexpression. HP14-19 was exposed to H2O2 to establish oxidative injury model. The cell viability with CXCR4 or CXCR7 overexpression was measured by MTT assay. Microplate reader was to evaluate the LDH and SOD levels. The expression of CXCR4 and CXCR7 receptor on HP14-19 was significantly higher after infection with adenovirus. Overexpression CXCR7 but not CXCR4 could enhance the proliferation of HP14-19. Overexpression of CXCR4 or CXCR7 significantly enhanced SDF-1 induced cell migration and cell survival rate of oxidative stress， in which CXCR7 showed a stronger migration effect. Compared with the control group， overexpression of CXCR4 or CXCR7 could reduce the LDH level and increased SOD activity caused by H2O2.The results suggested that overexpression of CXCR4 was involved in the proliferation of HP14-19 mediated by SDF-1， and both CXCR4 and CXCR7 mediated the SDF-1 induced migration and anti-oxidative stress of HP14-19.
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