J-N Yue1, W-M Li, W-Z Hong, J Yang, T Zhu, Y Fang, W-G Fu. 1. Department of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. fu.weiguo@zs-hospital.sh.cn.
Abstract
OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-210 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans (ASO) through the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. PATIENTS AND METHODS: In the present work, the vascular endothelial cells in ASO patients were selected as objects of study, the cell lines with miR-210 interference and overexpression were constructed with the Crisp/Case9 technique for subsequent experiments as experimental group, and the aortic endothelial cells of a healthy human were used as control group. First, the changes in the transcriptional and translational levels of such genes as JAK2 and STAT3 in the JAK-STAT signaling pathway in cell lines with miR-210 interference and overexpression were detected via fluorescence quantitative Polymerase Chain Reaction (qPCR) and Western blotting. The changes in the transcriptional and translational levels of nitric oxide synthase (NOS) in cells were detected in experimental group and control group to clarify the regulatory effect of miR-210 on the JAK-STAT signaling pathway. At the same time, the cell proliferation in experimental group and control group was observed via methyl thiazolyl tetrazolium (MTT) assay and the apoptosis rate was detected in both groups via flow cytometry. RESULTS: The results of fluorescence qPCR and Western blotting revealed that the expression level of miR-210 was significantly increased in cells of ASO patients compared with that in aortic endothelial cells of healthy human with a significant difference (p<0.05). At the same time, the inhibition on miR-210 could significantly reduce the transcriptional and translational levels of JAK2, STAT3, and NOS, block the JAK-STAT signaling pathway, suppress the cell proliferation, and promote apoptosis. The overexpression of miR-210 could markedly increase the transcriptional and translational levels of JAK2, STAT3, and NOS, activate the JAK-STAT signaling pathway, promote the cell proliferation, and suppress the apoptosis. CONCLUSIONS: MiR-210 can be involved in the apoptosis process of vascular endothelial cells in ASO through the JAK-STAT signaling pathway.
OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-210 on the apoptosis of vascular endothelial cells in arteriosclerosis obliterans (ASO) through the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. PATIENTS AND METHODS: In the present work, the vascular endothelial cells in ASO patients were selected as objects of study, the cell lines with miR-210 interference and overexpression were constructed with the Crisp/Case9 technique for subsequent experiments as experimental group, and the aortic endothelial cells of a healthy human were used as control group. First, the changes in the transcriptional and translational levels of such genes as JAK2 and STAT3 in the JAK-STAT signaling pathway in cell lines with miR-210 interference and overexpression were detected via fluorescence quantitative Polymerase Chain Reaction (qPCR) and Western blotting. The changes in the transcriptional and translational levels of nitric oxide synthase (NOS) in cells were detected in experimental group and control group to clarify the regulatory effect of miR-210 on the JAK-STAT signaling pathway. At the same time, the cell proliferation in experimental group and control group was observed via methyl thiazolyl tetrazolium (MTT) assay and the apoptosis rate was detected in both groups via flow cytometry. RESULTS: The results of fluorescence qPCR and Western blotting revealed that the expression level of miR-210 was significantly increased in cells of ASO patients compared with that in aortic endothelial cells of healthy human with a significant difference (p<0.05). At the same time, the inhibition on miR-210 could significantly reduce the transcriptional and translational levels of JAK2, STAT3, and NOS, block the JAK-STAT signaling pathway, suppress the cell proliferation, and promote apoptosis. The overexpression of miR-210 could markedly increase the transcriptional and translational levels of JAK2, STAT3, and NOS, activate the JAK-STAT signaling pathway, promote the cell proliferation, and suppress the apoptosis. CONCLUSIONS:MiR-210 can be involved in the apoptosis process of vascular endothelial cells in ASO through the JAK-STAT signaling pathway.