miR-129-5p inhibits oxidized low-density lipoprotein-induced A7r5 cell viability and migration by targeting HMGB1 and the PI3k/Akt signaling pathway.
miR-129-5p inhibits oxidized low-density lipoprotein-induced A7r5 cell viability and migration by targeting HMGB1 and the PI3k/Akt signaling pathway.
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DOI：
10.3892/etm.2022.11168
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发表时间：
2022-03
影响因子：
2.7
通讯作者：
Wu Y
中科院分区：
文献类型：
--
作者：
Jiang H;Gong R;Wu Y
基因治疗在心血管疾病治疗中的作用机制仍有待阐明。microRNAs（miRs）是血管平滑肌细胞的重要调控因子，参与动脉粥样硬化的形成。本研究旨在探讨miR-129- 5 p在高迁移率族蛋白1（HMGB 1）和PI 3 k/Akt信号通路中的调控作用，并进一步探讨miR-129- 5 p在氧化低密度脂蛋白（ox-LDL）诱导的A7 r5细胞存活和迁移中的作用。使用细胞计数试剂盒-8、集落形成、伤口愈合和Transwell测定法测定细胞活力、存活力和迁移。采用逆转录-定量PCR和Western blotting检测miR-129- 5 p和HMGB 1的表达水平。使用双荧光素酶测定来确认miR-129- 5 p和HMGB 1之间的关联。RT-qPCR结果显示，ox-LDL诱导的A7 r5细胞中miR-129- 5 p的表达水平较对照组显著降低。与对照组相比，ox-LDL诱导的A7 r5细胞的存活率和迁移率均增加。Western blot和RT-qPCR结果显示，miR-129- 5 p可降低A7 r5细胞中HMGB 1的表达。本研究结果表明，miR-129- 5 p可抑制ox-LDL诱导的A7 r5细胞的存活率、存活率和迁移率，并直接靶向HMGB 1调节PI 3 k/Akt信号通路。综上所述，miR-129- 5 p通过直接靶向HMGB 1抑制PI 3 k/Akt信号通路，降低ox-LDL诱导的A7 r5细胞的存活率、存活率和迁移率。
The mechanisms underlying gene therapy for the treatment of cardiovascular diseases remain to be elucidated. microRNAs (miRs) have been recognized as key regulators in vascular smooth muscle cells, which are involved in the formation of atherosclerosis. The present study aimed to explore the role of miR-129-5p in the regulation of high-mobility group box 1 protein (HMGB1) and the PI3k/Akt signaling pathway, and further explore the role of miR-129-5p in the viability and migration of A7r5 cells induced by oxidized low-density lipoprotein (ox-LDL). Cell viability, viability and migration were determined using Cell Counting Kit-8, colony formation, wound healing and Transwell assays. The expression levels of miR-129-5p and HMGB1 were detected using reverse transcription-quantitative PCR and western blotting. A dual-luciferase assay was used to confirm the association between miR-129-5p and HMGB1. RT-qPCR results in the present study demonstrated that the expression levels of miR-129-5p in A7r5 cells induced by ox-LDL were significantly decreased, compared with the control cells. Moreover, the viability and migration of A7r5 cells induced by ox-LDL were increased compared with control group. Western blot and RT-qPCR results showed that miR-129-5p decreased the expression of HMGB1 in A7r5 cells compared with control group. The present results demonstrated that miR-129-5p inhibited the viability, viability and migration of A7r5 cells induced by ox-LDL, and directly targeted HMGB1 to regulate the PI3k/Akt signaling pathway. In conclusion, miR-129-5p inhibited the PI3k/Akt signaling pathway by directly targeting HMGB1, and reduced the viability, viability and migration of A7r5 cells induced by ox-LDL.
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影响因子：
5.8
作者：
Madrigal-Matute, Julio;Rotllan, Noemi;Aranda, Juan F.;Fernandez-Hernando, Carlos
通讯作者：
Fernandez-Hernando, Carlos
影响因子：
3.7
作者：
Li, Weifeng;Zhi, Wenbing;Niu, Xiaofeng
通讯作者：
Niu, Xiaofeng
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影响因子：
2
作者：
Gu Y;Xiao ZH;Wu J;Guo M;Lv P;Dou N
通讯作者：
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影响因子：
6
作者：
Koshman, Yevgeniya E.;Patel, Nilamkumar;Chu, Miensheng;Iyengar, Rekha;Kim, Taehoon;Ersahin, Cagatay;Lewis, William;Heroux, Alain;Samarel, Allen M.
通讯作者：
Samarel, Allen M.
影响因子：
3.7
作者：
Chang TY;Tsai WC;Huang TS;Su SH;Chang CY;Ma HY;Wu CH;Yang CY;Lin CH;Huang PH;Cheng CC;Cheng SM;Wang HW
通讯作者：
Wang HW