Upregulating the renin-angiotensin system in bone marrow mesenchymal stem cells by hypoxia
- VernacularTitle:缺氧对骨髓间充质干细胞肾素血管紧张素系统表达的影响
- Author:
Rongrong XIAO
;
Jinghong GAO
;
Yue FAN
;
Lu ZHOU
;
Ruizhen SHI
;
Qingping LI
- Publication Type:Journal Article
- Keywords:
Renin-angiotensin system;
Bone marrow mesenchymal stem cell;
Hypoxia/serum deprivation
- From:
Journal of Medical Postgraduates
2015;(2):123-126
- CountryChina
- Language:Chinese
-
Abstract:
Objective The renin-angiotensin system ( RAS) is involved in myocardial anoxic injury .This study aimed to in-vestigate the expressions of AT 1-R, AT2-R, and angiotensin-converting enzyme ( ACE ) in bone marrow mesenchymal stem cells (MSCs) under hypoxia. Methods Rat MSCs were isolated, cultured, and identified with CD29 and CD11b/c antibodies.The is-chemic injury model was established by exposing the MSCs to hypoxia and serum deprivation ( Hypoxia/SD) for 24 hours, while the control cells were cultured in L-DMEM with 10%FBS.The vitality and apoptosis of the cells were detected by trypan blue staining , CCK8 assay, and Annexin V-FITC staining.The mRNA and protein expressions of AT 1-R, AT2-R, and ACE were determined by real-time quantitative PCR and Western blot , respectively. Results The positive rate of CD29 was >97%and that of CD11b/c was <1% in the MSCs.Compared with the control group, Hypoxia/SD significantly increased the rate of cell apoptosis ([6.73 ±0.78]%vs [19.93 ±4.92]%, P<0.01), decreased the rate of cell viability ([78.49 ±4.94]%vs [37.33 ±2.91]%, P<0.01), and up-regulated the mRNA and protein expressions of AT 1-R, AT2-R, and ACE. Conclusion Hypoxia/SD activates the RAS in MSCs and improves the protective function of the cells against myocardial anoxic injury .
