Protein kinase Cβ-mediated matrix metalloproteinase 9 activation by acute femoral artery injury
10.3760/cma.j.issn.0254-9026.2011.07.019
- VernacularTitle:蛋白激酶Cβ介导急性股动脉损伤后基质金属蛋白酶9的活化
- Author:
Wenwei WU
;
Chun HUANG
- Publication Type:Journal Article
- Keywords:
Protein kinase C-delta;
Matrix metalloproteinase 9,Endothelium,vascular
- From:
Chinese Journal of Geriatrics
2011;30(7):589-592
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the activation of matrix metalloproteinase (MMP)9 by acute arterial injury and the involved signaling mechanism in murine femoral artery. Methods In the C57BL/6 mice femoral artery denudation injury were performed. Total protein and membrane protein extracts were prepared from targeted arteries. The MMP 9 activity was measured by zymography assay, the expressions of MMP 9 antigen and protein kinase C (PKC) isoforms were measured by Western blot. Seventy-two hours after mice fed with PKCβ inhibitor (ruboxistaurin), the denudation injury triggered MMP 9 activation was reassessed. Results Within 4-24 hours after denudation injury, MMP 9 activity in femoral arteries was significantly increased, with a peak induction of (99.3±9.5) times the sham control (F=51.49,P＜0.01) at 8 h. MMP 9 antigen increased in parallel with MMP 9 activity. Within 15-120 minutes after denudation injury, there was a significant induction of PKCβⅡ in membrane fraction of femoral arteries, with a maximum induction of (7.50±0.60) times the sham control (F=207.06,P＜0.01)at 30 min. Injury-induced MMP 9 activation was significantly inhibited by ruboxistaurin. Conclusions MMP 9 activation is, at least in part, mediated by PKCβ in acute arterial denudation injury, it highlights the new target for therapeutic intervention to suppress the over-activation of MMP 9, which plays a critical role in restenosis.
