Upregulation of MicroRNA-210 Regulates Renal Angiogenesis Mediated by Activation of VEGF Signaling Pathway under Ischemia/Perfusion Injury in vivo and in vitro

Kidney and Blood Pressure Research - Tập 35 Số 3 - Trang 182-191 - 2012
Yong Li1, Yuanlei Lou, Jue Wu, Qiongfang Ruan, An Xie, Fei Guo, Cui Su-ping, Zhifeng Deng, Yang Wang
1Institute of Urology, Nanchang University, Nanchang, China

Tóm tắt

<i>Background:</i> MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs that regulate gene expression and function, but little is known about regulation of miRNAs in the kidneys under normal or pathologic conditions. Here, we sought to investigate the potential involvement of miRNAs in renal ischemia/reperfusion (I/R) injury and angiogenesis and to define some of the miRNAs possibly associated with renal angiogenesis. <i>Methods and Results:</i> Male Balb/c mice were subjected to a standard renal I/R. CD31 immunostaining indicated a significant increase of microvessels in the ischemic region. VEGF and VEGFR2 expression were increased in renal I/R at both the mRNA and protein levels which were detected by qRT-PCR and Western blot, respectively. More importantly, 76 microRNAs exhibited more than 2-fold changes using Agilent microRNA microarray, which contains downregulation of 40 miRNAs and upregulation of 36 miRNAs. Upregulation of miR-210 was confirmed by qRT-PCR with prominent changes at 4 and 24 h after reperfusion. Furthermore, overexpression of miR-210 in HUVEC-12 cells enhances VEGF and VEGFR2 expression and promotes angiogenesis on Matrigel in vitro. <i>Conclusion:</i> These findings suggest miR-210 may be involved in targeting the VEGF signaling pathway to regulate angiogenesis after renal I/R injury, which provides novel insights into the angiogenesis mechanism of renal I/R injury.

Từ khóa


Tài liệu tham khảo

10.1038%2Fsj.ki.5002312

10.1016%2Fj.ijsu.2006.06.001

10.5483%2FBMBRep.2008.41.4.278

10.1016%2Fj.yexcr.2005.11.012

10.1161%2FCIRCULATIONAHA.108.814145

10.1161%2FCIRCRESAHA.107.153916

10.1126%2Fscience.1174381

10.1016%2Fj.devcel.2008.07.008

10.1038%2Fnature02871

10.1038%2Fnrg1379

10.2215%2FCJN.00520109

10.1093%2Fcvr%2Fcvp015

10.1016%2Fj.jocn.2009.10.009

10.1089%2Fomi.2009.0035

10.1016%2Fj.febslet.2008.05.048

10.1172%2FJCI37829

10.1152%2Fajprenal.00184.2005

10.1038%2Fki.1991.175

10.1038%2Fki.1995.483

10.1093%2Fndt%2Fgfm774

10.1093%2Fnar%2Fgni178

10.1371%2Fjournal.pone.0000116

10.1016%2Fj.febslet.2008.05.048

10.1016%2Fj.mvr.2010.08.001

10.1681%2FASN.2009070718

10.1097%2FMNH.0b013e32831ec1db

10.1074%2Fjbc.272.51.32521

10.1074%2Fjbc.M800731200

10.1186%2F1476-4598-7-56

10.1016%2Fj.tcm.2007.03.003

10.1016%2Fj.mcn.2008.01.013

10.1089%2Flrb.2008.1011

Thông tin
Thông tin xuất bản

Kidney and Blood Pressure Research

Tập 35 Số 3

182-191

Thông tin tác giả