MicroRNA-17-5p通过靶向ANKH促进血管钙化。

IF 2 4区 医学 Q3 CLINICAL NEUROLOGY Current neurovascular research Pub Date : 2022-03-16 DOI:10.2174/1567202619666220316115425
Chao Shi, Jiaorong Tan, Jian-can Lu, Junling Huang, Xiangqi Li, Jiahong Xu, Xing Wang
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引用次数: 0

摘要

背景微小RNA(miRNA)可能参与血管钙化的过程。然而,微小RNA-17-5p在血管钙化中的作用尚未阐明。在这项研究中,我们展示了微小RNA-17-5p对血管钙化的影响。材料和方法使用Lipofectamine 2000用miR-17-5p模拟物、miR-17-5p抑制剂或阴性对照(NC)转染血管平滑肌细胞(VSMCs)。然后用成骨培养基诱导细胞。测定了碱性磷酸酶(ALP)活性和矿化度。用逆转录聚合酶链反应测定骨钙素(OC)、骨形态发生蛋白2(BMP-2)、Col1agren Ia(Colla)、Runx2和强直蛋白同源物(ANKH)基因的表达。血管钙化是使用肾功能衰竭模型发展起来的。结果miR-17-5p模拟物转染后ALP活性增加,而miR-17-5p抑制剂降低了ALP活性(p<0.05)。miR-17-5p模拟物组的矿物结数量和平均面积大于相应的对照组和NC组(p<0.05),与对照组和NC组相比,miR-17-5p模拟物组的Col1a和Runx2更高。ANKH的表达在使用miR-17-5p模拟物的VSMCs中降低,而在使用miR17-5p抑制剂的VSMC中增加。ANKH siRNA干预也促进矿化。钙化主动脉中miR-17-5p表达上调,ANKH表达下调。结论miR-17-5p可能通过抑制ANKH的表达来促进血管钙化。
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MicroRNA-17-5p promotes vascular calcification by targeting ANKH.
BACKGROUND MicroRNAs (miRNAs) may participate in the process of vascular calcification. However, the role of microRNA-17-5p in vascular calcification has not been clarified. In this study, we showed the effects of microRNA-17-5p on vascular calcification. MATERIALS AND METHODS Vascular smooth muscle cells (VSMCs) were transfected with miR-17-5p mimics, an miR-17-5p inhibitor or a negative control (NC) using Lipofectamine 2000. Then the cells were induced by an osteogenic medium. Alkaline phosphatase (ALP) activity and mineralization were determined. Osteocalcin (OC), bone morphogenetic protein 2(BMP-2), Col1agren Ia (Colla), Runx2 and ankylosis protein homolog (ANKH) gene expressions were determined by reverse transcription-polymerase chain reaction. Vascular calcification was developed using a renal failure model. RESULTS The ALP activity was increased when miR-17-5p mimics were transfected, whereas the miR-17-5p inhibitor reduced ALP activity (p < 0.05). The number and average area of mineral node in miR-17-5p mimics group were larger than those in corresponding control and NC groups (p < 0.05). The number and average area of the mineral nodes in the miR-17-5p inhibitor group were smaller than those in corresponding control and NC groups (p < 0.05). Bmp2, OC, Col1a and Runx2 were higher in the miR-17-5p mimics group compared to those in the control and NC groups. ANKH expression was decreased in VSMCs with the miR-17-5p mimics and increased in VSMCs with miR-17-5p inhibitor. ANKH siRNA intervention also promoted mineralization. The miR-17-5p expression was upregulated and ANKH was down-regulated in the aortic arteries with calcification. CONCLUSION Our data showed that miR-17-5p may promote vascular calcification by inhibiting ANKH expression.
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来源期刊
Current neurovascular research
Current neurovascular research 医学-临床神经学
CiteScore
3.80
自引率
9.50%
发文量
54
审稿时长
3 months
期刊介绍: Current Neurovascular Research provides a cross platform for the publication of scientifically rigorous research that addresses disease mechanisms of both neuronal and vascular origins in neuroscience. The journal serves as an international forum publishing novel and original work as well as timely neuroscience research articles, full-length/mini reviews in the disciplines of cell developmental disorders, plasticity, and degeneration that bridges the gap between basic science research and clinical discovery. Current Neurovascular Research emphasizes the elucidation of disease mechanisms, both cellular and molecular, which can impact the development of unique therapeutic strategies for neuronal and vascular disorders.
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