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Tytuł:
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MicroRNA-23a suppresses the apoptosis of inflammatory macrophages and foam cells in atherogenesis by targeting HSP90.
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Autorzy:
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Qiao Y; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Wang C; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Translational Medicine Center of Northern China, Harbin Medical University, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Kou J; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Wang L; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Han D; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Huo D; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Li F; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Zhou X; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Meng D; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Xu J; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Murtaza G; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Artyom B; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China.
Ma N; Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China; Key Laboratory of Cardiovascular Medicine Research (Harbin Medical University), Ministry of Education, Harbin, China; Medical Science Institute of Hei Longjiang Province, Harbin, China. Electronic address: .
Luo S; Department of Gerontology, The First Hospital of Harbin Medical University, Harbin, China. Electronic address: .
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Źródło:
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Gene [Gene] 2020 Mar 01; Vol. 729, pp. 144319. Date of Electronic Publication: 2019 Dec 26.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Amsterdam, Elsevier/North-Holland, 1976-
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MeSH Terms:
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Atherosclerosis/*genetics
Atherosclerosis/*pathology
Foam Cells/*pathology
HSP90 Heat-Shock Proteins/*genetics
Macrophages/*pathology
MicroRNAs/*genetics
3' Untranslated Regions ; Apoptosis/genetics ; Atherosclerosis/metabolism ; Cell Proliferation/genetics ; Foam Cells/metabolism ; Humans ; Inflammation/genetics ; Macrophages/metabolism ; MicroRNAs/metabolism ; NF-kappa B/metabolism ; THP-1 Cells
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Contributed Indexing:
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Keywords: Apoptosis; HSP90; Inflammatory response; miR-23a
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Substance Nomenclature:
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0 (3' Untranslated Regions)
0 (HSP90 Heat-Shock Proteins)
0 (MIRN23a microRNA, human)
0 (MicroRNAs)
0 (NF-kappa B)
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Entry Date(s):
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Date Created: 20191230 Date Completed: 20200227 Latest Revision: 20200612
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Update Code:
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20240104
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DOI:
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10.1016/j.gene.2019.144319
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PMID:
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31884108
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In previous study, we have found that microRNA-23a is down regulated in atherosclerotic tissues. Here we demonstrate that miR-23a directly binds to 3'UTR of HSP90 mRNA to suppress the expression of HSP90. To investigate the potential roles of miR-23a in macrophage, THP-1 macrophages were transfected with miR-23a mimics or inhibitors. Our results showed inflammatory factors IL-6 and MCP-1 concentrations in cell culture medium of macrophage and foam cell transfected with miR-23a mimics were decreased. Furthermore, we find that apoptosis of macrophage and foam cells transfected with miR-23a mimics were inhibited. Over expression of miR-23a in foam cells could reduced lipid intake and accumulation in foam cells. Meanwhile, we found that in inflammatory macrophages and foam cells transfected with miR-23a mimcs, HSP90 and NF-κB proteins are significantly decreased. Our results have suggested a promising and potential therapeutic target for atherosclerosis.
(Copyright © 2019 Elsevier B.V. All rights reserved.)