Effects of renal ischemia on microRNAs and VEGF-NOTCH signal moleculars in mice
10.3760/cma.j.issn.1671-0282.2011.04.010
- VernacularTitle:肾缺血对缺氧诱导microRNAs及VEGF-NOTCH信号分子的影响
- Author:
Fen LIU
;
Jue WU
;
Yuanlei LOU
;
Qiongfang RUAN
;
Yong LI
;
Suping CUI
;
Yang WANG
- Publication Type:Journal Article
- Keywords:
microRNA;
Angiogenesis;
Kindey;
Ischemia;
VEGF;
Notch gene
- From:
Chinese Journal of Emergency Medicine
2011;20(4):380-384
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression changes of microRNAs and VEGF-NOTCH in renal ischemic injury in mice, and to explore the potential mechanism associated with renal angiogenesis.Method Male Balb/c mice were subjected to a standard renal ischemia to induce acute kidney injury (AKI) after 45 min of bilateral renal artery clamping. Following 4 h, 24 h of reperfusion or sham operation, kindey tissues were collected and subjected to detect the expression changes of microRNAs which relatived with angiogenesis and VEGF, Flk-1, Notch1 mRNA by Quantitative Real-time RT-PCR. Flk-1 protein was detected by Western blotting analysis at 24 h and 72 h following Ischemia/Reperfusion(I/R) injury. The expression of CD31 was examined in tissue sections by immunohistochemistry staining, and the microvessels in ischemic region of each group were counted. Results miRNA-210 and miRNA-92a expression increased significantly, with prominent changes at 4 h and 24 h after reperfusion( P ＜ 0.05 ). VEGF and Flk-1 mRNA expression and Flk-1 protein were increased in renal I/R compared with control group respectively (P＜0.05 ).Immunohistochemistry staining results of CD31 showed a significant increase of microvessels in renal ischemic region. Conclusion This study first reported the changes in miRNAs expression in response to kidney I/R in mouse. our results implied that miRNAs may be involved in targeting VEGF-Notch pathway signaling to regulate angiogenesis after renal I/R injury. It provided novel insights into the angiogenesis mechanism of renal ischemic injury.
