Mechanism of Flk-1~+ MSC alleviating injury in the mouse model of renal ischemia-reperfusion
- VernacularTitle:肾缺血-再灌注损伤模型中Flk-1~+间质干细胞参与损伤修复的机制研究
- Author:
Qin HAN
;
Kanghua LI
;
Dongnan HE
;
Chunhua ZHAO
- Publication Type:Journal Article
- Keywords:
Mesenchymal stem cell;
Ischemia-reperfusion;
Stem cell transplantation
- From:
Journal of Medical Postgraduates
2003;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the mechanism underlying the repairing effect of Flk-1+ MSC on injury.Methods: We established the mouse model of acute renal ischemia-reperfusion,perfused murine Flk-1+ MSC within 1 hour or after 10 days in the acute and chronic groups,respectively,determined the homing of GFP positive Flk-1+ MSCs and the percentage of proliferating cells in the injured renal tissues by immunohistochemistry,and identified chronic fibrosis after injury by Masson trichrome staining. Results: Tissue injury and inflammation were significantly alleviated in the acute group,exhibiting a good long-term recovery,but no significant improvement was observed in the chronic group.The number of PCNA positive cells reached the peak at 3 days in the acute group,as compared with 10 days in the control,indicating that MSC engraftment effected an earlier endogenous repair.GFP staining showed that most of the MSCs homed to the interstitial region and the rest to the renal tubule.Conclusion: Flk-1+ MSC has a repairing effect on renal injury via alleviating acute inflammation and launching endogenous repair,while direct differentiation from Flk-1+ MSC is not the primary mechanism of its therapeutic efficacy.
