Mmu-miR-351 attenuates the survival of cardiac arterial endothelial cells through targeting STAT3 in the atherosclerotic mice.
The signal transducer and activator of transcription 3 (STAT3) signaling pathway was involved in regulation of endothelial cell survival/apoptosis and was regarded as a target for prevention of atherosclerosis or other cardiovascular diseases. Factors, regulating STAT3 expression and activity, have aroused a wide range of interest, such as miRNAs or transcription factors. The aim of this study is to explore the role of miR-351, a miRNA found not long before, in the regulation of STAT3 expression and endothelial cell survival in the model mice with atherosclerosis (AS). Expression of miR-351 in the serum and cardiac arterial endothelial cells of the WT mice and AS mice was detected. Real-time qPCR analysis showed that miR-351 was upregulated in the serum and endothelial cells of the AS mice, displaying an opposite expression pattern with STAT3. To explore the role and mechanism of miR-351 in the endothelial cell survival, the miR-351 mimic was transfected in to the endothelial cells. MTT and Trypan Blue assays showed miR-351 attenuated the survival of endothelial cells. Our results of the TargetScan output and the 3'UTR luciferase reporter assay indicated that STAT3 was target of miR-351. Additionally, miR-351 resisted the elevation of STAT3 protein level and promotion of endothelial cell survival caused by SD19. Finally, our in vitro angiogenesis assay revealed that miR-351 suppressed angiogenesis and resisted the promotion of angiogenesis caused by SD19. In conclusion, miR-351 was upregulated in the atherosclerotic mice. MiR-351 can attenuate the survival of endothelial cells and suppress angiogenesis through targeting STAT3 in vitro.
Department of Cardiology, Tianjin Chest Hospital, Tianjin, China. Electronic address: yingz_cardio@163.com.
Ying
Y
Zhang
Department of Cardiology, Tianjin Chest Hospital, Tianjin, China.
Yujie
Y
Liu
Department of Cardiology, Tianjin Chest Hospital, Tianjin, China.
Hong
H
Zhang
Department of Cardiology, Tianjin Chest Hospital, Tianjin, China.
Minghui
M
Wang
Department of Cardiology, Tianjin Chest Hospital, Tianjin, China.
Jinlian
J
Zhang
D000818:Animals; D050197:Atherosclerosis / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D002470:Cell Survival; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D005786:Gene Expression Regulation; D053614:Janus Kinase 2 / Q000378:metabolism; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D009389:Neovascularization, Pathologic / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D050796:STAT3 Transcription Factor / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction
C580764:MIRN351 microRNA, 351; D035683:MicroRNAs; D050796:STAT3 Transcription Factor; D053614:Janus Kinase 2
Atherosclerosis (AS); STAT3; miR-351