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Short Time Tripterine Treatment Enhances Endothelial Progenitor Cell Function via Heat Shock Protein 32
Author(s) -
Lu Chenhui,
Zhang Xiaoping,
Zhang Denghai,
Pei Erli,
Xu Jichong,
Tang Tao,
Ye Meng,
Uzan Georges,
Zhi Kangkang,
Li Maoquan,
Zuo Keqiang
Publication year - 2015
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24849
Subject(s) - endothelial progenitor cell , progenitor cell , chemistry , in vivo , transplantation , celastrol , endothelial stem cell , pharmacology , cancer research , apoptosis , microbiology and biotechnology , in vitro , stem cell , medicine , biology , biochemistry
The dysfunction of endothelial progenitor cells (EPCs) limits their potential for the treatment of ischemia and atherosclerosis. Therefore, we investigated the effect of tripterine on EPC function and examined the underlying mechanisms. The effect of tripterine, an active component of Tripterygium wilfordii Hook, on the enhancement of EPC function and the efficiency of EPC transplantation was investigated in vitro and in vivo. Treatment of EPCs with tripterine at 2.5 µM for 4 h inhibited oxidized low‐density lipoprotein (ox‐LDL) induced ROS production, cell apoptosis, and cell senescence and improved the migration and tube formation capacities of EPCs treated with ox‐LDL (200 µg/ml). In vivo studies showed that tripterine conditioning of EPCs administered to ischemic foci improved blood perfusion and microvascular density in a mouse hindlimb ischemia model. Examination of the underlying mechanisms indicated that the effect of tripterine is mediated by the induction of heat shock protein 32 expression and the inhibition of JNK activation. The present results are of clinical significance because they suggest the potential of tripterine as a therapeutic agent to improve the efficacy of EPC transplantation for the treatment of ischemic diseases. J. Cell. Physiol. 230: 1139–1147, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company