Overexpressed CD59 inhibits complement-induced damage to bone marrow mesenchymal stem cells
10.16571/j.cnki.1008-8199.2017.12.013
- VernacularTitle:过表达CD59抑制补体对骨髓间充质干细胞的损伤作用
- Author:
Kai XIAO
1
;
hua Zhen FANG
;
feng Xin GAO
;
jing Jing ZHAO
;
kun Ruo HUANG
;
Ming XIE
Author Information
1. 华中科技大学同济医学院附属普爱医院足踝外科
- Keywords:
Bone marrow mesenchymal stem cells;
Complement;
Autologous transplantation;
Complement membrane attack complex
- From:
Journal of Medical Postgraduates
2017;30(12):1289-1294
- CountryChina
- Language:Chinese
-
Abstract:
Objective Studies are rarely reported on how to avoid complement system attack during the transplantation of bone marrow mesenchymal stem cells (BMSCs).We explored the effect of the overexpression of CD59 on complement membrane attack-induced damage to rat BMSCs (rBMSCs) during autologous transplantation.Methods BMSCs from SD rats were cultured and treated with CD59 overexpression plasmid or rBMSC empty vector or left untreated,followed by detection of the expression of CD59 in the rBMSCs by flow cytometry.Then the rBMSCs were incubated with autologous rat serum (ARS),inactivated ARS (iARS),CD59+ARS,or CD59+iARS or not incubated.The cytotoxicity of the serum complement on the rBMSCs was observed by PI staining and the apoptosis of the rBMSCs determined by flow cytometry.Results The expression of CD59 was significantly higher in the rBMSCs treated with CD59 than in those untreated (7,4.9% vs 50.5%,P<0.05).The apop tosis rate was remarkably lower in the rBMSCs not incubated ([8.4± 1.1] %) and those incubated with CD59+ARS ([19.1 ±3.1] %) than in those incubated with ARS ([40.3±4.3] %) (P<0.05).The deposition of the complement membrane attack complex was significantly decreased in the rBMSCs not incubated (50.1%) and those incubated with CD59+ARS (71.0%) as compared with those incubated with ARS (99.7%) (P<0.05).The apoptosis rate of the rBMSCs treated with CD59 was markedly lower than that of those left untreated (P<0.05).Conclusion The overexpression of CD59 inhibits the damage induced by complement to rBMSCs by reducing the formation of the complement membrane attack complex during autologous transplantation.