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Title:
Role of hsa_circ_0000280 in regulating vascular smooth muscle cell function and attenuating neointimal hyperplasia via ELAVL1 | Cellular and Molecular Life Sciences
Description:
The pathological proliferation of cells in vascular smooth muscle underlies neointimal hyperplasia (NIH) development during atherosclerosis. Circular RNAs (circRNAs), which represent novel functional biomarkers and RNA-binding proteins, contribute to multiple cardiovascular diseases; however, their roles in regulating the vascular smooth muscle cell cycle remain unknown. Thus, we aimed to identify the roles of circRNAs in vascular smooth muscle during coronary heart disease (CHD). Through circRNA sequencing of CHD samples and human antigen R (ELAVL1) immunoprecipitation, we identified circRNAs that are associated with CHD and interact with ELAVL1. Our results suggested that the hsa_circ_0000280 associated with CHD inhibits cell proliferation and induces ELAVL1-dependent cell cycle arrest. Gain/loss-of-function experiments and assays in vivo indicated that hsa_circ_0000280 facilitates interactions between ELAVL1 and cyclin-dependent kinase suppressor 1 (CDKN1A) mRNA and stabilization of this complex and leads to cell cycle arrest at the G1/S checkpoint, inhibiting cell proliferation of vascular smooth muscle cells in vitro and NIH in vivo. Importantly, hsa_circ_0000280 reduced neointimal thickness and smooth muscle cell proliferation in vivo. Taken together, these findings reveal a novel pathway in which hsa_circ_0000280 facilitates the regulation of ELAVL1 on CDKN1A mRNA to inhibit NIH. Therefore, measuring and modulating their expression might represent a potential diagnostic or therapeutic strategy for CHD.
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Keywords {๐}
hsacirc, elavl, cell, fig, article, cdkna, google, scholar, cas, circrnas, evector, vascular, cycle, expression, rna, proliferation, tests, student, smooth, muscle, mrna, hasmcs, protein, chd, cells, circular, coronary, results, hur, data, neointimal, human, supplementary, res, hyperplasia, wang, zhang, rnas, compared, exogenous, function, cdk, control, cardiovascular, levels, controls, heart, binding, progression, study,
Topics {โ๏ธ}
lncrna oip5-as1 increase fine-tune ฮฑ-sma expression pdgf-bb-induced hasmcs drives cell-cycle progression bb-induced hasmc model vascular smooth muscle article download pdf binds u-rich sequences suppressing pdgfrฮฒ-erk signaling smooth muscle cells quantitative rt-pcr analysis virus aav9-sm22a-circ_280 rna-binding protein hur harvested cdkn1a rt-pcr ฮฑ-sma positive cells rip-agarose gel electrophoresis english language editing coronary heart disease rip-rt-qpcr result facilitating hur-repressed functions intimal/media thickness measurements aav9-sm22a-circ_280 group elavl1-oip5-as1 cyclin-dependent kinase 2 cyclin-dependent kinase monitoring ribosomal rna mir100hg preferentially promotes cell cycle progression main cellular targets circular rnas open residual wounded area elavl1 rip-circrna sequencing privacy choices/manage cookies attenuating neointimal hyperplasia pdgf-bb atherosclerotic cardiovascular disease cell cycle arrest rna-binding protein 3สน-end poly circular rna enriched graph shows quantitation rna-binding activity cell cycle transition smc cell cycle cell proliferation depends cell cycle analysis rt-pcr analysis human coronary vessels neointimal area stained circular rna purification
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headline:Role of hsa_circ_0000280 in regulating vascular smooth muscle cell function and attenuating neointimal hyperplasia via ELAVL1
description:The pathological proliferation of cells in vascular smooth muscle underlies neointimal hyperplasia (NIH) development during atherosclerosis. Circular RNAs (circRNAs), which represent novel functional biomarkers and RNA-binding proteins, contribute to multiple cardiovascular diseases; however, their roles in regulating the vascular smooth muscle cell cycle remain unknown. Thus, we aimed to identify the roles of circRNAs in vascular smooth muscle during coronary heart disease (CHD). Through circRNA sequencing of CHD samples and human antigen R (ELAVL1) immunoprecipitation, we identified circRNAs that are associated with CHD and interact with ELAVL1. Our results suggested that the hsa_circ_0000280 associated with CHD inhibits cell proliferation and induces ELAVL1-dependent cell cycle arrest. Gain/loss-of-function experiments and assays in vivo indicated that hsa_circ_0000280 facilitates interactions between ELAVL1 and cyclin-dependent kinase suppressor 1 (CDKN1A) mRNA and stabilization of this complex and leads to cell cycle arrest at the G1/S checkpoint, inhibiting cell proliferation of vascular smooth muscle cells in vitro and NIH in vivo. Importantly, hsa_circ_0000280 reduced neointimal thickness and smooth muscle cell proliferation in vivo. Taken together, these findings reveal a novel pathway in which hsa_circ_0000280 facilitates the regulation of ELAVL1 on CDKN1A mRNA to inhibit NIH. Therefore, measuring and modulating their expression might represent a potential diagnostic or therapeutic strategy for CHD.
datePublished:2022-12-07T00:00:00Z
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Circular RNA
RNA-binding protein
Neointimal hyperplasia
Atherosclerosis
Coronary heart disease
Cell Biology
Biomedicine
general
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Biochemistry
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headline:Role of hsa_circ_0000280 in regulating vascular smooth muscle cell function and attenuating neointimal hyperplasia via ELAVL1
description:The pathological proliferation of cells in vascular smooth muscle underlies neointimal hyperplasia (NIH) development during atherosclerosis. Circular RNAs (circRNAs), which represent novel functional biomarkers and RNA-binding proteins, contribute to multiple cardiovascular diseases; however, their roles in regulating the vascular smooth muscle cell cycle remain unknown. Thus, we aimed to identify the roles of circRNAs in vascular smooth muscle during coronary heart disease (CHD). Through circRNA sequencing of CHD samples and human antigen R (ELAVL1) immunoprecipitation, we identified circRNAs that are associated with CHD and interact with ELAVL1. Our results suggested that the hsa_circ_0000280 associated with CHD inhibits cell proliferation and induces ELAVL1-dependent cell cycle arrest. Gain/loss-of-function experiments and assays in vivo indicated that hsa_circ_0000280 facilitates interactions between ELAVL1 and cyclin-dependent kinase suppressor 1 (CDKN1A) mRNA and stabilization of this complex and leads to cell cycle arrest at the G1/S checkpoint, inhibiting cell proliferation of vascular smooth muscle cells in vitro and NIH in vivo. Importantly, hsa_circ_0000280 reduced neointimal thickness and smooth muscle cell proliferation in vivo. Taken together, these findings reveal a novel pathway in which hsa_circ_0000280 facilitates the regulation of ELAVL1 on CDKN1A mRNA to inhibit NIH. Therefore, measuring and modulating their expression might represent a potential diagnostic or therapeutic strategy for CHD.
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Circular RNA
RNA-binding protein
Neointimal hyperplasia
Atherosclerosis
Coronary heart disease
Cell Biology
Biomedicine
general
Life Sciences
Biochemistry
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name:The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan City, China
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name:The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan City, China
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