Role of endoplasmic reticulum stress in the biological functions of MCP-1-induced mesenchymal stem cells
会议名称：《中国生理学会第23届全国会员代表大会暨生理学学术大会》
会议日期：2010年
学科分类：0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种]
摘 要：正Background:Mesenchymal stem cells（MSCs） are pluripotent cells with promising therapeutic potential. Injection of MSCs decreases ischemia/reperfusion injury mainly through paracrine *** chemotactic protein-1（MCP-1） plays an important role in ischaemia/reperfusion injury and transplant *** reticulum（ER） stress is a protective cell response that repairs mild injured cells and sacrifices severely injured cells. We previously found MCP-1 is harmful to transplants in ***,it is beneficial when used to stimulate MSC in vitro before MSC is *** present study observed the role of RR on MCP-1-induced changes of MSC biological ***:Mesenchymal stem cells were isolated from rat bone marrow and treated with MCP- 1（10 ng/mL） with or without pretreatment of ER protein *** protein inhibitors used were Zinc protoporphyrin （ZnPP,an HO-1 inhibitor）,C/EBP homologous protein specific short interfering RNA（CHOP siRNA） or activating transcription factor-6 specific short interfering RNA（ATF-6 siRNA）.The cell function of proliferation, invasion and migration and mechanisms were analyzed by functional assays and western ***:HO-1 promoted cell growth and migration but inhibited cell apoptosis and adhesion independent of other ERS proteins. Without other treatment,siRNA of ERS protein CHOP or ATF-6 inhibited MSC migration but inducing apoptosis and have no effects on cell adhesion and *** siRNA induced ATF-6 ***-6 siRNA induced CHOP protein expression,indicating a bilateral compensation of CHOP and *** above treatments have no effect on HO-1 protein amount,indicating HO-1 is not the down stream molecule of other ER ***-1 induced MSC migration and adhesion while inhibited MSC *** effects of MCP-1 on MSCs were blocked by CHOP or ATF-6 ***:in vitro prestimulation of MSC with MCP-1 will promote beneficial effect while prevent harmful effect of MSC in vivo thr