Long non-coding RNA MALAT1 sponges miR-30c to promote the calcification of human vascular smooth muscle cells by regulating Runx2

作者全名："Gong, Ying; Zhong, Qing; Xia, Yunfeng; Wen, Yang; Gan, Hua"

作者地址："[Gong, Ying; Zhong, Qing; Xia, Yunfeng; Wen, Yang; Gan, Hua] Chongqing Med Univ, Affiliated Hosp 1, Chongqing, Peoples R China; [Gan, Hua] Chongqing Med Univ, Affiliated Hosp 1, Dept Nephrol, 1 Youyi Rd, Chongqing 400016, Peoples R China"

通信作者："Gan, H (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Nephrol, 1 Youyi Rd, Chongqing 400016, Peoples R China."

来源：RENAL FAILURE

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000975155200001

JCR分区：Q1

影响因子：3

年份：2023

卷号：45

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：Vascular calcification; MALAT1; miR-30c; vascular smooth muscle cells

摘要："Objectives Recent evidence suggested that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play critical roles in the pathogenesis of vascular calcification (VC). In this study, we tried to explore the expression and role of a lncRNA, i.e., metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and a miRNA, i.e., miR-30c, in VC. Methods In vitro VC model was induced in human vascular smooth muscle cells (VSMCs) after 10 days culture in calcifying medium containing 2 mM Na2HPO4. Alizarin red S staining, calcium assay and western blot analysis of runt-related transcription factor 2 (Runx2) and alpha smooth muscle actin (alpha-SMA) were performed to evaluate VC. Knockdown of MALAT1 and up-regulation of MALAT1, miR-30c and Runx2 was performed to determine the impact of these molecules on VSMCs calcification. Dual-luciferase report assay was performed to confirm the relationship between MALAT1 and miR-30c or miR-30c and Runx2. In addition, quantitative reverse transcription PCR and western blot were used to determine gene and protein expression. Results MALAT1 was increased, while miR-30c was decreased in calcified VSMCs. Knockdown of MALAT1 suppressed VSMCs calcification; on the contrary, up-regulation of MALAT1 promoted VSMCs calcification. The effect of MALAT1 over-expression on VSMCs calcification was reversed by upregulation of miR-30c, which was reversed again by upregulation of Runx2. Dual-luciferase report assay confirmed that there is a direct interaction between MALAT1 and miR-30c, and Runx2 is a direct target of miR-30c. Conclusion MALAT1 over-expression promoted VSMCs calcification, which was at least partially through regulating the miR-30c/Runx2 axis."

基金机构：Chongqing Health Commission [2022WSJK012]

基金资助正文：This work was supported by the Chongqing Health Commission under grant of 2022WSJK012.