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Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease
This study is aimed at exploring the role and potential molecular mechanism of microRNA-21 (miR-21) in coronary heart disease (CHD). RT-qPCR analysis was conducted to detect the expression of miR-21, Sprouty 1 (SPRY1), and connexin 43 (CX43). The protein expression of SPRY1 and CX43 was measured by...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8643245/ https://www.ncbi.nlm.nih.gov/pubmed/34873417 http://dx.doi.org/10.1155/2021/6942699 |
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author | Liu, Wei Li, Yilin Zhao, Dongming |
author_facet | Liu, Wei Li, Yilin Zhao, Dongming |
author_sort | Liu, Wei |
collection | PubMed |
description | This study is aimed at exploring the role and potential molecular mechanism of microRNA-21 (miR-21) in coronary heart disease (CHD). RT-qPCR analysis was conducted to detect the expression of miR-21, Sprouty 1 (SPRY1), and connexin 43 (CX43). The protein expression of SPRY1 and CX43 was measured by western blot. ELISA was performed for measuring inflammatory factors, including intercellular adhesion molecule-1 (ICAM-1) and interleukin-1 beta (IL-1β). The target relationship between miR-21 and SPRY1 was determined by dual-luciferase reporter assay. Cell multiplication and apoptosis were detected using CCK-8 assay and flow cytometry analysis, respectively. Our results indicated that miR-21, CX43, and the level of inflammatory cytokines including ICAM-1 and IL-1β were upregulated, while SPRY1 was downregulated in blood samples from CHD patients compared with the controls. Besides, miR-21 directly targeted SRPY-1. miR-21 could suppress SPRY1 expression and enhance CX43 expression in VSMCs. Moreover, miR-21 accelerated cell multiplication and attenuated cell apoptosis in VSMCs. Collectively, these findings suggested that miR-21 could effectively elevate VSMC multiplication and repress apoptosis by targeting SPRY1 in CHD, providing a potential target for therapeutic strategy of CHD. |
format | Online Article Text |
id | pubmed-8643245 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-86432452021-12-05 Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease Liu, Wei Li, Yilin Zhao, Dongming Comput Math Methods Med Research Article This study is aimed at exploring the role and potential molecular mechanism of microRNA-21 (miR-21) in coronary heart disease (CHD). RT-qPCR analysis was conducted to detect the expression of miR-21, Sprouty 1 (SPRY1), and connexin 43 (CX43). The protein expression of SPRY1 and CX43 was measured by western blot. ELISA was performed for measuring inflammatory factors, including intercellular adhesion molecule-1 (ICAM-1) and interleukin-1 beta (IL-1β). The target relationship between miR-21 and SPRY1 was determined by dual-luciferase reporter assay. Cell multiplication and apoptosis were detected using CCK-8 assay and flow cytometry analysis, respectively. Our results indicated that miR-21, CX43, and the level of inflammatory cytokines including ICAM-1 and IL-1β were upregulated, while SPRY1 was downregulated in blood samples from CHD patients compared with the controls. Besides, miR-21 directly targeted SRPY-1. miR-21 could suppress SPRY1 expression and enhance CX43 expression in VSMCs. Moreover, miR-21 accelerated cell multiplication and attenuated cell apoptosis in VSMCs. Collectively, these findings suggested that miR-21 could effectively elevate VSMC multiplication and repress apoptosis by targeting SPRY1 in CHD, providing a potential target for therapeutic strategy of CHD. Hindawi 2021-11-27 /pmc/articles/PMC8643245/ /pubmed/34873417 http://dx.doi.org/10.1155/2021/6942699 Text en Copyright © 2021 Wei Liu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Liu, Wei Li, Yilin Zhao, Dongming Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title | Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title_full | Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title_fullStr | Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title_full_unstemmed | Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title_short | Modulation of Vascular Smooth Muscle Cell Multiplication, Apoptosis, and Inflammatory Damage by miR-21 in Coronary Heart Disease |
title_sort | modulation of vascular smooth muscle cell multiplication, apoptosis, and inflammatory damage by mir-21 in coronary heart disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8643245/ https://www.ncbi.nlm.nih.gov/pubmed/34873417 http://dx.doi.org/10.1155/2021/6942699 |
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