Bo-Ya Zhang1, Zhe Jin2, Zhuo Zhao3. 1. Department of Cardiology, Tianjin Nankai Hospital, Nankai, Tianjin, 300070, China. 2. Department of Clinical, Tianjin Nankai Hospital, Dongli, Tianjin, 300100, China. 3. Department of Toxicology, Tianjin Entry Exit Inspection and Quarantine Bureau, Dongli, Tianjin, 300000, China. Electronic address: zhaozhuo_burberry@126.com.
Abstract
BACKGROUND: Apoptosis in vascular endothelial cells (VECs) are closely correlated to multiple endotheliocyte-related cardiovascular diseases, for example atherosclerosis. Long non-coding RNAs (lncRNAs) have been testified to play important role in regulation of VECs. The purpose of this study is to investigate the potential regulation of lncRNA long intergenic noncoding RNA 00305 (LINC00305) on hypoxia induced VECs. METHODS: Human umbilical vein endothelial cells (HUVECs) were respectively induced with normoxia or hypoxia (1%). Expression levels of lncRNA and miRNA were detected using RT-PCR. Proliferation ability was tested by CCK-8 assay. Apoptosis assay were performed using flow cytometry and TUNEL staining. Target miRNAs prediction was performed using bioinformatics analysis. RESULTS: LINC00305 expression was significantly up-regulated in hypoxia induce HUVECs. Gain- and loss-of-function experiments showed that LINC00305 enhanced expression suppressed the proliferation and enhanced the apoptosis of HUVECs, while LINC00305 lower-expression exerted the opposite effect. Bioinformatics analysis revealed that miR-136 targeted LINC00305 art 3'-UTR. Moreover, rescue experiment confirmed the reversing function of miR-136 to LINC00305 on HUVECs proliferation and apoptosis. CONCLUSION: Our study revealed the apoptosis-promoting role of LINC00305 in hypoxia-induced HUVECs via acting as miR-136 sponge, suggesting the vital function of lncRNAs on VECs apoptosis.
BACKGROUND: Apoptosis in vascular endothelial cells (VECs) are closely correlated to multiple endotheliocyte-related cardiovascular diseases, for example atherosclerosis. Long non-coding RNAs (lncRNAs) have been testified to play important role in regulation of VECs. The purpose of this study is to investigate the potential regulation of lncRNA long intergenic noncoding RNA 00305 (LINC00305) on hypoxia induced VECs. METHODS:Human umbilical vein endothelial cells (HUVECs) were respectively induced with normoxia or hypoxia (1%). Expression levels of lncRNA and miRNA were detected using RT-PCR. Proliferation ability was tested by CCK-8 assay. Apoptosis assay were performed using flow cytometry and TUNEL staining. Target miRNAs prediction was performed using bioinformatics analysis. RESULTS:LINC00305 expression was significantly up-regulated in hypoxia induce HUVECs. Gain- and loss-of-function experiments showed that LINC00305 enhanced expression suppressed the proliferation and enhanced the apoptosis of HUVECs, while LINC00305 lower-expression exerted the opposite effect. Bioinformatics analysis revealed that miR-136 targeted LINC00305 art 3'-UTR. Moreover, rescue experiment confirmed the reversing function of miR-136 to LINC00305 on HUVECs proliferation and apoptosis. CONCLUSION: Our study revealed the apoptosis-promoting role of LINC00305 in hypoxia-induced HUVECs via acting as miR-136 sponge, suggesting the vital function of lncRNAs on VECs apoptosis.
Authors: Margherita A C Pomatto; Chiara Gai; Maria Chiara Deregibus; Ciro Tetta; Giovanni Camussi Journal: Int J Endocrinol Date: 2018-04-01 Impact factor: 3.257