High glucose promotes atherosclerosis by regulating miRNA let7d‐5p level
ABSTRACT Background MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains unknown how let7d‐5p contributes to the process of atherosclerosis. Methods Twenty fresh tissues and a total of 28 wax block specimens from...
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Published in | Journal of diabetes investigation Vol. 15; no. 6; pp. 711 - 724 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Japan
John Wiley & Sons, Inc
01.06.2024
John Wiley and Sons Inc Wiley |
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Abstract | ABSTRACT
Background
MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains unknown how let7d‐5p contributes to the process of atherosclerosis.
Methods
Twenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d‐5p was assessed using quantitative RT‐PCR (qRT‐PCR). A series of in vitro experiments was used to determine the roles of let7d‐5p knockdown and overexpression in vascular smooth muscle cells (VSMCs).
Results
We discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d‐5p. In VSMCs, the expression of miRNA let7d‐5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d‐5p, whereas the opposite was true when let7d‐5p was inhibited, according to gain and loss of function studies. Mechanically, let7d‐5p might activate the GSK3β/β‐catenin signaling pathway via binding to the high mobility group AT‐Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP‐1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d‐5p levels.
Conclusions
High glucose stimulated the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d‐5p.
In this study, we reported that the miR let7d‐5p expression was decreased in the carotid plaque of patients with diabetes. We first revealed high glucose promoted the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may alleviate atherosclerosis via up‐regulating miR let7d‐5p levels. GLP‐1RA liraglutide could inhibit the proliferation and migration of VSMCs by up‐regulating the level of let7d‐5p. |
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AbstractList | MiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown how let7d-5p contributes to the process of atherosclerosis.
Twenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d-5p was assessed using quantitative RT-PCR (qRT-PCR). A series of in vitro experiments was used to determine the roles of let7d-5p knockdown and overexpression in vascular smooth muscle cells (VSMCs).
We discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d-5p. In VSMCs, the expression of miRNA let7d-5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d-5p, whereas the opposite was true when let7d-5p was inhibited, according to gain and loss of function studies. Mechanically, let7d-5p might activate the GSK3β/β-catenin signaling pathway via binding to the high mobility group AT-Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP-1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d-5p levels.
High glucose stimulated the proliferation and migration of VSMCs by regulating the let7d-5p/HMGA2/GSK3β/β-catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d-5p. MiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown how let7d-5p contributes to the process of atherosclerosis.BACKGROUNDMiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown how let7d-5p contributes to the process of atherosclerosis.Twenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d-5p was assessed using quantitative RT-PCR (qRT-PCR). A series of in vitro experiments was used to determine the roles of let7d-5p knockdown and overexpression in vascular smooth muscle cells (VSMCs).METHODSTwenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d-5p was assessed using quantitative RT-PCR (qRT-PCR). A series of in vitro experiments was used to determine the roles of let7d-5p knockdown and overexpression in vascular smooth muscle cells (VSMCs).We discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d-5p. In VSMCs, the expression of miRNA let7d-5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d-5p, whereas the opposite was true when let7d-5p was inhibited, according to gain and loss of function studies. Mechanically, let7d-5p might activate the GSK3β/β-catenin signaling pathway via binding to the high mobility group AT-Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP-1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d-5p levels.RESULTSWe discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d-5p. In VSMCs, the expression of miRNA let7d-5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d-5p, whereas the opposite was true when let7d-5p was inhibited, according to gain and loss of function studies. Mechanically, let7d-5p might activate the GSK3β/β-catenin signaling pathway via binding to the high mobility group AT-Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP-1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d-5p levels.High glucose stimulated the proliferation and migration of VSMCs by regulating the let7d-5p/HMGA2/GSK3β/β-catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d-5p.CONCLUSIONSHigh glucose stimulated the proliferation and migration of VSMCs by regulating the let7d-5p/HMGA2/GSK3β/β-catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d-5p. BackgroundMiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown how let7d-5p contributes to the process of atherosclerosis.MethodsTwenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d-5p was assessed using quantitative RT-PCR (qRT-PCR). A series of in vitro experiments was used to determine the roles of let7d-5p knockdown and overexpression in vascular smooth muscle cells (VSMCs).ResultsWe discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d-5p. In VSMCs, the expression of miRNA let7d-5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d-5p, whereas the opposite was true when let7d-5p was inhibited, according to gain and loss of function studies. Mechanically, let7d-5p might activate the GSK3β/β-catenin signaling pathway via binding to the high mobility group AT-Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP-1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d-5p levels.ConclusionsHigh glucose stimulated the proliferation and migration of VSMCs by regulating the let7d-5p/HMGA2/GSK3β/β-catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d-5p. ABSTRACT Background MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains unknown how let7d‐5p contributes to the process of atherosclerosis. Methods Twenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d‐5p was assessed using quantitative RT‐PCR (qRT‐PCR). A series of in vitro experiments was used to determine the roles of let7d‐5p knockdown and overexpression in vascular smooth muscle cells (VSMCs). Results We discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d‐5p. In VSMCs, the expression of miRNA let7d‐5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d‐5p, whereas the opposite was true when let7d‐5p was inhibited, according to gain and loss of function studies. Mechanically, let7d‐5p might activate the GSK3β/β‐catenin signaling pathway via binding to the high mobility group AT‐Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP‐1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d‐5p levels. Conclusions High glucose stimulated the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d‐5p. ABSTRACT Background MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains unknown how let7d‐5p contributes to the process of atherosclerosis. Methods Twenty fresh tissues and a total of 28 wax block specimens from carotid endarterectomy procedures were obtained from the Luoyang Central Hospital affiliated to Zhengzhou University. The expression of let7d‐5p was assessed using quantitative RT‐PCR (qRT‐PCR). A series of in vitro experiments was used to determine the roles of let7d‐5p knockdown and overexpression in vascular smooth muscle cells (VSMCs). Results We discovered that the carotid plaques from diabetic patients had lower expression levels of miR let7d‐5p. In VSMCs, the expression of miRNA let7d‐5p was significantly lower in high glucose conditions compared with low glucose situations. The proliferation and migration of VSMCs were also inhibited by the overexpression of let7d‐5p, whereas the opposite was true when let7d‐5p was inhibited, according to gain and loss of function studies. Mechanically, let7d‐5p might activate the GSK3β/β‐catenin signaling pathway via binding to the high mobility group AT‐Hook 2 (HMGA2) mRNA in VSMCs. Additionally, GLP‐1RA liraglutide may prevent the migration and proliferation of VSMCs by raising let7d‐5p levels. Conclusions High glucose stimulated the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may slow atherosclerosis by increasing the levels of miR let7d‐5p. In this study, we reported that the miR let7d‐5p expression was decreased in the carotid plaque of patients with diabetes. We first revealed high glucose promoted the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may alleviate atherosclerosis via up‐regulating miR let7d‐5p levels. GLP‐1RA liraglutide could inhibit the proliferation and migration of VSMCs by up‐regulating the level of let7d‐5p. In this study, we reported that the miR let7d‐5p expression was decreased in the carotid plaque of patients with diabetes. We first revealed high glucose promoted the proliferation and migration of VSMCs by regulating the let7d‐5p/HMGA2/GSK3β/β‐catenin pathway, and liraglutide may alleviate atherosclerosis via up‐regulating miR let7d‐5p levels. GLP‐1RA liraglutide could inhibit the proliferation and migration of VSMCs by up‐regulating the level of let7d‐5p. |
Author | Guo, Yiting Zhang, Yanfang Zhao, Songfeng Li, Xuan Liu, Fentao Wang, Yunlong Mai, Peipei Su, Jie Zhao, Wenyu Wang, Hua Wen, Zhiguo |
AuthorAffiliation | 4 Department of Vascular Surgery Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China 3 Department of Endocrinology Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China 5 Henan Bioengineering Research Center Zhengzhou City Henan Province China 6 Zhongyuan Scholars Workstation of Henan Luoyang City Henan Province China 1 Department of Ultrasonography Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China 2 ABclonal Technology Company Wuhan Hubei Province China |
AuthorAffiliation_xml | – name: 4 Department of Vascular Surgery Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China – name: 6 Zhongyuan Scholars Workstation of Henan Luoyang City Henan Province China – name: 5 Henan Bioengineering Research Center Zhengzhou City Henan Province China – name: 2 ABclonal Technology Company Wuhan Hubei Province China – name: 1 Department of Ultrasonography Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China – name: 3 Department of Endocrinology Luoyang Central Hospital Affiliated to Zhengzhou University Luoyang City Henan Province China |
Author_xml | – sequence: 1 givenname: Hua surname: Wang fullname: Wang, Hua organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 2 givenname: Fentao surname: Liu fullname: Liu, Fentao organization: ABclonal Technology Company – sequence: 3 givenname: Wenyu surname: Zhao fullname: Zhao, Wenyu organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 4 givenname: Yiting orcidid: 0000-0001-9546-6476 surname: Guo fullname: Guo, Yiting organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 5 givenname: Peipei surname: Mai fullname: Mai, Peipei organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 6 givenname: Songfeng surname: Zhao fullname: Zhao, Songfeng organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 7 givenname: Zhiguo surname: Wen fullname: Wen, Zhiguo organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 8 givenname: Jie surname: Su fullname: Su, Jie organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 9 givenname: Xuan surname: Li fullname: Li, Xuan organization: Luoyang Central Hospital Affiliated to Zhengzhou University – sequence: 10 givenname: Yunlong surname: Wang fullname: Wang, Yunlong organization: Zhongyuan Scholars Workstation of Henan – sequence: 11 givenname: Yanfang orcidid: 0000-0002-1999-3079 surname: Zhang fullname: Zhang, Yanfang email: yanfangz@zzu.edu.cn organization: Zhongyuan Scholars Workstation of Henan |
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Copyright | 2024 The Authors. published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd. 2024 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd. 2024. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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Snippet | ABSTRACT
Background
MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains... MiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown how... ABSTRACT Background MiRNA let7d‐5p has been recently reported to be abnormally expressed in diabetes‐associated atherosclerosis (AS). However, it still remains... BackgroundMiRNA let7d-5p has been recently reported to be abnormally expressed in diabetes-associated atherosclerosis (AS). However, it still remains unknown... In this study, we reported that the miR let7d‐5p expression was decreased in the carotid plaque of patients with diabetes. We first revealed high glucose... |
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StartPage | 711 |
SubjectTerms | Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Atherosclerosis - metabolism beta Catenin - genetics beta Catenin - metabolism Blood vessels Cell Movement Cell Proliferation Cells, Cultured Diabetes Diabetes mellitus Female Genotype & phenotype Glucose Glucose - metabolism Glycogen Synthase Kinase 3 beta - genetics Glycogen Synthase Kinase 3 beta - metabolism High mobility group proteins HMGA2 Protein - genetics HMGA2 Protein - metabolism Humans Hyperglycemia Male MicroRNAs MicroRNAs - genetics Middle Aged miRNA MiRNA let7d‐5p mRNA Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Original Signal Transduction Smooth muscle Type 2 diabetes mellitus β-Catenin |
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Title | High glucose promotes atherosclerosis by regulating miRNA let7d‐5p level |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjdi.14180 https://www.ncbi.nlm.nih.gov/pubmed/38483136 https://www.proquest.com/docview/3062829926 https://www.proquest.com/docview/2957167942 https://pubmed.ncbi.nlm.nih.gov/PMC11143425 https://doaj.org/article/f4951f040e7d43aa836b4c753ec97fa8 |
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