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间充质干细胞分泌的血管内皮生长因子对心肌细胞的保护作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2013年第1期
页码:
17-021
栏目:
基础研究
出版日期:
2013-02-25

文章信息/Info

Title:
Effect of vascular endothelial growth factor from mesenchymal stem cells on antiapoptosis of H9C2 cells through PI3K/Akt signal pathway
作者:
毛洪波1; 邹赛1; 唐俊明2; 3; 王家宁2; 孔霞2; 郑飞2; 杨建业2
(1.竹溪县人民医院内科，湖北 竹溪 442300；湖北医药学院：2.附属人民医院临床医学研究所，3.生理学教研室，湖北 十堰 442000)
Author(s):
MAO Hongbo1;  ZOU Sai1;  TANG Junming2; 3;  WANG Jianing2;  KONG Xia2;  ZHENG Fei2;  YANG Jianye2
(1.Department of Cardiology, Zhuxi People’s Hospital, Zhuxi 442300, Hubei, China; 2.Institute of Clinical Medicine, People’s Hospital, 3.Department of Physiology, Hubei University of Medicine, Shiyan 442000, Hubei, Chin)
关键词:
间充质干细胞; H9C2细胞; 血管内皮生长因子; 凋亡; PI3K/Akt
Keywords:
mesenchymal stem cells;  H9C2;  vascular endothelial growth factor;  apoptosis;  PI3K/Akt
分类号:
Q25；R542.2
DOI:
-
文献标识码:
A
摘要:
目的:探索间充质干细胞通过其分泌的血管内皮生长因子对H9C2细胞的保护作用及机制。方法： 收集骨髓源间充质干细胞的条件培养基，分别处理培养，将其置于缺氧小室缺氧处理21 h，复氧处理6 h。阻断实验利用VEGFR阻断剂SU5416与间充质干细胞的条件培养基共处理。随后，利用流式细胞术ANNEXIN/PI双标法分析其凋亡变化。Western blotting分析H9C2细胞pAkt的表达。结果： RTPCR结果显示间充质干细胞表达血管内皮生长因子,Western blotting结果显示间充质干细胞条件培养基增加了H9C2细胞pAkt的水平。AnnexinV/PI分析发现间充质干细胞条件培养基明显降低了H9C2细胞缺氧复氧的凋亡，且这种抗凋亡作用能被VEGFR阻断剂SU5416或PI3K/Akt途径阻断剂LY294002所阻断。结论： 间充质干细胞通过其分泌的血管内皮生长因子通过激活PI3K/Akt途径保护H9C2细胞。
Abstract:
AIM:To explore the effect of vascular endothelial growth factor (VEGF) from mesenchymal stem cells (MSCs) on antiapoptosis of H9C2 cells. METHODS: In vitro, condition medium (CM) from MSCs was collected after MSCs were cultured for 2 days. After H9C2 cells were pretreated with VEGFR inhibitor SU5416 (5 μmol/L) or PI3K/Akt inhibitor LY294002 (10 μmol/L) for 1 h, apoptosis of the cells was observed under hypoxia with Annexin V and PI double staining by flow cytometry. The expressions of Akt and pAkt in H9c2 cells were detected by Western blotting and expressions of VEGF in MSCs were detected by RTPCR. RESULTS: RTPCR showed the expression of VEGF on MSCs, and Western blotting showed increased levels of pAkt protein in H9C2 cells after treatment with CM. CM decreased H9C2 cell apoptosis but the antiapoptotic effect of the CM was blocked by VEGFR inhibitor SU5416 or PI3K/Akt inhibitor LY294002 (10 μmol/L), respectively. CONCLUSION: VEGF from MSCs plays an important role in the protection of H9C2 cells through PI3K/Akt signal pathway.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2011-12-19.基金项目：国家自然科学基金项目资助(81170095;30700306) 通讯作者：唐俊明，副教授，主要从事干细胞移植治疗心肌梗死机制研究Email: tangjm416@163.com 作者简介：毛洪波，主治医师Email:104815371@qq.com
更新日期/Last Update: 2013-03-20