Murine Cytomegalovirus Infection Induced miR-1929-3p Down-Regulation Promotes the Proliferation and Apoptosis of Vascular Smooth Muscle Cells in Mice by Targeting Endothelin A Receptor and Downstream NLRP3 Activation Pathway

被引:0
作者
Lijuan He
Wei Zhou
Lamei Wang
Na Tang
Yongjia Wang
Hua Zhong
Yan Tang
Dongmei Xi
Fang He
机构
[1] Medical College of Shihezi University,NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases and Key Laboratory of Education Ministry of Xinjiang Endemic and Ethnic Diseases
[2] Medical College of Shihezi University,Centre of Medical Functional Experiments
[3] The First Affiliated Hospital of Medical College of Shihezi University,Department of Geriatrics
来源
Molecular Biotechnology | 2023年 / 65卷
关键词
Vascular smooth muscle cell; Murine cytomegalovirus; miR-1929-3p; NLRP3 inflammasome; Endothelin receptor type A;
D O I
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学科分类号
摘要
Our previous study demonstrated in vivo that mouse cytomegalovirus (MCMV) infection promoted vascular remodeling after downregulation of miR-1929-3p. This study aimed to investigate the role of miR-1929-3p/ETAR/NLRP3 pathway in mouse vascular smooth muscle cells (MOVAS) after MCMV infection. First, PCR was used to detect the success of the infection. Second, MOVAS were transfected with the miR-1929-3p mimic, inhibitor, and ETAR overexpressed adenovirus vector. Cell proliferation was detected using EdU, whereas apoptosis was detected using flow cytometry. The expression of miR-1929-3p and ETAR were detected using qRT-PCR. Western blot detected proteins of cell proliferation, apoptosis, and the NLRP3 inflammasome. Interleukin-1β and interleukin-18 were determined using ELISA. The results revealed that after 48 h, MCMV infection promoted the proliferation of MOVAS when the MOI was 0.01. MCMV infection increased ETAR by downregulating miR-1929-3p. The miR-1929-3p mimic reversed the proliferation and apoptosis, whereas the miR-1929-3p inhibitor promoted this effect. ETAR overexpression further promoted MCMV infection by downregulating miR-1929-3p-mediated proliferation and apoptosis. MCMV infection mediates the downregulation of miR-1929-3p and the upregulation of ETAR, which activates NLRP3 inflammasome. In conclusion, MCMV infection promoted the proliferation of MOVAS, possibly by downregulating miR-1929-3p, promoting the upregulation of the target gene ETAR and activating NLRP3 inflammasome.
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页码:1954 / 1967
页数:13
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