PPARγ enhances invasive capacity of endothelial progenitor cells via up-regulation of cathepsin L

王强; 余洁; 赵刚; 卢巍; 邓梦杨; 康华利; 黄岚

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PPARγ enhances invasive capacity of endothelial progenitor cells via up-regulation of cathepsin L

更新时间：2026-01-09

- PPARγ enhances invasive capacity of endothelial progenitor cells via up-regulation of cathepsin L
- Journal of Army Medical University Vol. 36, Issue 16, Pages: 1643-1646(2014)
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  CLC： R322.12;R329.28;R394.3
- Published：2014
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王强,余洁,赵刚,卢巍,邓梦杨,康华利,黄岚.过氧化物酶增殖激活受体γ通过上调组织蛋白酶L表达增强内皮祖细胞的侵袭能力[J].陆军军医大学学报(原第三军医大学学报),2014,36(16):1643-1646.

　Wang Qiang,Yu Jie,Zhao Gang,Lu Wei,Deng Mengyang,Kang Huali,Huang Lan.PPARγ enhances invasive capacity of endothelial progenitor cells via up-regulation of cathepsin L[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(16):1643-1646.
王强,余洁,赵刚,卢巍,邓梦杨,康华利,黄岚.过氧化物酶增殖激活受体γ通过上调组织蛋白酶L表达增强内皮祖细胞的侵袭能力[J].陆军军医大学学报(原第三军医大学学报),2014,36(16):1643-1646. DOI：

　Wang Qiang,Yu Jie,Zhao Gang,Lu Wei,Deng Mengyang,Kang Huali,Huang Lan.PPARγ enhances invasive capacity of endothelial progenitor cells via up-regulation of cathepsin L[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(16):1643-1646. DOI：

摘要

目的观察过氧化物酶增殖激活受体γ（peroxisome proliferator-activated receptor-γ， PPARγ）激活后对内皮祖细胞（endothelial progenitor cells， EPCs）侵袭能力的影响并探讨其分子机制。方法分离和培养大鼠骨髓源性EPCs，分别用PPARγ激动剂罗格列酮（0、1、5、10 μmol/L）、PPARγ拮抗剂GW9662（5 μmol/L）或组织蛋白酶L（cathepsin L）抑制剂Z-FF-FMK（10 μmol/L）干预EPCs后，采用基质胶侵袭实验检测EPCs的侵袭能力；半定量RT-PCR、Western blot检测cathepsin L mRNA和蛋白的表达。结果 PPARγ激动剂罗格列酮（1~10 μmol/L）呈剂量依赖增强EPCs的侵袭能力、上调EPCs中cathepsin L的mRNA和蛋白表达（P0.05，P0.01），而PPARγ拮抗剂GW9662（5 μmol/L）可削弱罗格列酮（10 μmol/L）上调cathepsin L mRNA和蛋白表达的作用（P0.01）；此外，GW9662（5 μmol/L）或cathepsin L抑制剂Z-FF-FMK（10 μmol/L）均可明显减弱罗格列酮（10 μmol/L）促进EPCs侵袭的作用（P0.01）。结论 PPARγ激活后通过上调cathepsin L表达增强EPCs的侵袭能力。

Abstract

Objective To observe the effect of peroxisome proliferator-activated receptor-γ (PPARγ) activation on the invasive capacity of endothelial progenitor cells (EPCs) and explore the underlying mechanism. Methods The rat bone marrow-derived EPCs isolated and cultured in vitro were treated with PPARγ agonist rosiglitazone (0

and 10 μmol/L)

PPARγ antagonist GW9662 (5 μmol/L) or cathepsin L inhibitor Z-FF-FMK (10 μmol/L). The invasive capacity of EPCs was evaluated by Matrigel invasion assay. The mRNA and protein expression of cathepsin L were analyzed by semi-quantitative RT-PCR and Western blotting. Results Treatment of PPARγ agonist rosiglitazone increased the invasive capacity of EPCs in a dose-dependent manner (P0.05

P0.01). The mRNA and protein expression of cathepsin L were up-regulated by rosiglitazone in a concentration-dependent manner (P0.05

P0.01)

which was blocked by PPARγ antagonist GW9662 (5 μmol/L) (P0.01). In addition

pretreatment of EPCs with GW9662 (5 μmol/L) or cathepsin L inhibitor Z-FF-FMK (10 μmol/L) attenuated rosiglitazone-promoted EPCs invasion (P0.01). Conclusion These findings demonstrate that the activation of PPARγ may enhance the invasive capacity of EPCs via up-regulating cathepsin L expression.

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