Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2
Several miRNAs have been demonstrated to be involved in endothelial dysfunction during atherosclerosis (AS). However, the detailed roles and underlying mechanisms of miR-34a in AS-associated endothelial cell apoptosis are far from being addressed. Apolipoprotein E-deficient (ApoE −/− ) mice fed with...
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description | Several miRNAs have been demonstrated to be involved in endothelial dysfunction during atherosclerosis (AS). However, the detailed roles and underlying mechanisms of miR-34a in AS-associated endothelial cell apoptosis are far from being addressed. Apolipoprotein E-deficient (ApoE
−/−
) mice fed with high-fat diet (HFD) were used as in vivo model of AS. Oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) were applied as in vitro model of AS. The effects of miR-34a on atherosclerotic lesions were evaluated by hematoxylin–eosin (HE) and Oil Red O staining. Pecam-1
+
endothelial cells were isolated from the aortic arch with flow cytometry. qRT-PCR and western blot were employed to measure gene and protein expression. The effects of miR-34a on cell viability, cell cycle distribution, and apoptosis were assessed by Cell counting kit (CCK)-8 and flow cytometry analysis. The relationship between miR-34a and Bcl-2 was confirmed by online softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP). miR-34a was upregulated in HFD-induced ApoE
−/−
mice and ox-LDL-treated HAECs. Anti-miR-34a decreased atherosclerotic lesions and inhibited Pecam-1
+
endothelial cells apoptosis in HFD-induced ApoE
−/−
mice. Moreover, anti-miR-34a significantly promoted cell viability, alleviated cell cycle arrest, and restrained apoptosis in ox-LDL-treated HAECs. Furthermore, Bcl-2 was identified as a target of miR-34a, and miR-34a inhibited Bcl-2 expression via binding to its 3′UTR. Rescue experiments demonstrated that Bcl-2 overexpression dramatically reversed miR-34a-mediated inhibition of cell growth and promotion of apoptosis in ox-LDL-exposed HAECs. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy. |
doi_str_mv | 10.1007/s00380-018-1169-6 |
format | Article |
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−/−
) mice fed with high-fat diet (HFD) were used as in vivo model of AS. Oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) were applied as in vitro model of AS. The effects of miR-34a on atherosclerotic lesions were evaluated by hematoxylin–eosin (HE) and Oil Red O staining. Pecam-1
+
endothelial cells were isolated from the aortic arch with flow cytometry. qRT-PCR and western blot were employed to measure gene and protein expression. The effects of miR-34a on cell viability, cell cycle distribution, and apoptosis were assessed by Cell counting kit (CCK)-8 and flow cytometry analysis. The relationship between miR-34a and Bcl-2 was confirmed by online softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP). miR-34a was upregulated in HFD-induced ApoE
−/−
mice and ox-LDL-treated HAECs. Anti-miR-34a decreased atherosclerotic lesions and inhibited Pecam-1
+
endothelial cells apoptosis in HFD-induced ApoE
−/−
mice. Moreover, anti-miR-34a significantly promoted cell viability, alleviated cell cycle arrest, and restrained apoptosis in ox-LDL-treated HAECs. Furthermore, Bcl-2 was identified as a target of miR-34a, and miR-34a inhibited Bcl-2 expression via binding to its 3′UTR. Rescue experiments demonstrated that Bcl-2 overexpression dramatically reversed miR-34a-mediated inhibition of cell growth and promotion of apoptosis in ox-LDL-exposed HAECs. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.</description><identifier>ISSN: 0910-8327</identifier><identifier>EISSN: 1615-2573</identifier><identifier>DOI: 10.1007/s00380-018-1169-6</identifier><identifier>PMID: 29704100</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>3' Untranslated regions ; Aortic arch ; Apolipoprotein E ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Bcl-2 protein ; Biomedical Engineering and Bioengineering ; Cardiac Surgery ; Cardiology ; CD31 antigen ; Cell cycle ; Cell growth ; Cholecystokinin ; Cytometry ; Endothelial cells ; Flow cytometry ; Gene expression ; High fat diet ; Immunoprecipitation ; Lesions ; Low density lipoprotein ; Medicine ; Medicine & Public Health ; Mice ; Oils & fats ; Original Article ; Ribonucleic acid ; RNA ; Target recognition ; Vascular Surgery</subject><ispartof>Heart and vessels, 2018-10, Vol.33 (10), p.1185-1194</ispartof><rights>Springer Japan KK, part of Springer Nature 2018</rights><rights>Heart and Vessels is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-3a14ae3a01869f2758f7634dc2b76536779c79097cfab40b8caa0f3f96c8274c3</citedby><cites>FETCH-LOGICAL-c396t-3a14ae3a01869f2758f7634dc2b76536779c79097cfab40b8caa0f3f96c8274c3</cites><orcidid>0000-0002-4240-4586</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00380-018-1169-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00380-018-1169-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29704100$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Gang</creatorcontrib><creatorcontrib>Sun, Guangli</creatorcontrib><creatorcontrib>Liu, Hai</creatorcontrib><creatorcontrib>Shu, Liliang</creatorcontrib><creatorcontrib>Liang, Zhenxing</creatorcontrib><title>Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2</title><title>Heart and vessels</title><addtitle>Heart Vessels</addtitle><addtitle>Heart Vessels</addtitle><description>Several miRNAs have been demonstrated to be involved in endothelial dysfunction during atherosclerosis (AS). However, the detailed roles and underlying mechanisms of miR-34a in AS-associated endothelial cell apoptosis are far from being addressed. Apolipoprotein E-deficient (ApoE
−/−
) mice fed with high-fat diet (HFD) were used as in vivo model of AS. Oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) were applied as in vitro model of AS. The effects of miR-34a on atherosclerotic lesions were evaluated by hematoxylin–eosin (HE) and Oil Red O staining. Pecam-1
+
endothelial cells were isolated from the aortic arch with flow cytometry. qRT-PCR and western blot were employed to measure gene and protein expression. The effects of miR-34a on cell viability, cell cycle distribution, and apoptosis were assessed by Cell counting kit (CCK)-8 and flow cytometry analysis. The relationship between miR-34a and Bcl-2 was confirmed by online softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP). miR-34a was upregulated in HFD-induced ApoE
−/−
mice and ox-LDL-treated HAECs. Anti-miR-34a decreased atherosclerotic lesions and inhibited Pecam-1
+
endothelial cells apoptosis in HFD-induced ApoE
−/−
mice. Moreover, anti-miR-34a significantly promoted cell viability, alleviated cell cycle arrest, and restrained apoptosis in ox-LDL-treated HAECs. Furthermore, Bcl-2 was identified as a target of miR-34a, and miR-34a inhibited Bcl-2 expression via binding to its 3′UTR. Rescue experiments demonstrated that Bcl-2 overexpression dramatically reversed miR-34a-mediated inhibition of cell growth and promotion of apoptosis in ox-LDL-exposed HAECs. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.</description><subject>3' Untranslated regions</subject><subject>Aortic arch</subject><subject>Apolipoprotein E</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Bcl-2 protein</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Cardiac Surgery</subject><subject>Cardiology</subject><subject>CD31 antigen</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cholecystokinin</subject><subject>Cytometry</subject><subject>Endothelial cells</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>High fat diet</subject><subject>Immunoprecipitation</subject><subject>Lesions</subject><subject>Low density lipoprotein</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Oils & fats</subject><subject>Original Article</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Target recognition</subject><subject>Vascular Surgery</subject><issn>0910-8327</issn><issn>1615-2573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kUFr3DAQhUVJabab_IBcgiCXXtSOJFuyjmmatIGFQGjPQtbKuw625Eg2YfvrK7O7CRRykUDzzZt5eghdUPhKAeS3BMArIEArQqlQRHxACypoSVgp-QlagKJAKs7kKfqc0hMALRVVn9ApUxKKLLFAf3-EFx_dZurM2AaPQ4P79pHwwuAhhj6MLmHn12Hcuq41Hbau6_Amhpdxi41f4zQNQ3QpZcwMYRhDahNuPTa5IYZku_nMT_UOH6f4Df5uO8LO0MfGdMmdH-4l-nN3-_vmF1k9_Ly_uV4Ry5UYCTe0MI6b7FKohsmyaqTgxdqyWoqSCymVlQqUtI2pC6graww0vFHCVkwWli_Rl71uNvQ8uTTqvk2zD-NdmJJmwFkBRcVlRq_-Q5_CFH3ebqaoYPlHq0zRPWWztxRdo4fY9ibuNAU9B6P3wei8sp6D0SL3XB6Up7p369eOYxIZYHsg5ZLfuPg2-n3VfxAnmTU</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Su, Gang</creator><creator>Sun, Guangli</creator><creator>Liu, Hai</creator><creator>Shu, Liliang</creator><creator>Liang, Zhenxing</creator><general>Springer Japan</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4240-4586</orcidid></search><sort><creationdate>20181001</creationdate><title>Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2</title><author>Su, Gang ; Sun, Guangli ; Liu, Hai ; Shu, Liliang ; Liang, Zhenxing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-3a14ae3a01869f2758f7634dc2b76536779c79097cfab40b8caa0f3f96c8274c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>3' Untranslated regions</topic><topic>Aortic arch</topic><topic>Apolipoprotein E</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Bcl-2 protein</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Cardiac Surgery</topic><topic>Cardiology</topic><topic>CD31 antigen</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cholecystokinin</topic><topic>Cytometry</topic><topic>Endothelial cells</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>High fat diet</topic><topic>Immunoprecipitation</topic><topic>Lesions</topic><topic>Low density lipoprotein</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Oils & fats</topic><topic>Original Article</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Target recognition</topic><topic>Vascular Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Su, Gang</creatorcontrib><creatorcontrib>Sun, Guangli</creatorcontrib><creatorcontrib>Liu, Hai</creatorcontrib><creatorcontrib>Shu, Liliang</creatorcontrib><creatorcontrib>Liang, Zhenxing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Heart and vessels</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Gang</au><au>Sun, Guangli</au><au>Liu, Hai</au><au>Shu, Liliang</au><au>Liang, Zhenxing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2</atitle><jtitle>Heart and vessels</jtitle><stitle>Heart Vessels</stitle><addtitle>Heart Vessels</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>33</volume><issue>10</issue><spage>1185</spage><epage>1194</epage><pages>1185-1194</pages><issn>0910-8327</issn><eissn>1615-2573</eissn><abstract>Several miRNAs have been demonstrated to be involved in endothelial dysfunction during atherosclerosis (AS). However, the detailed roles and underlying mechanisms of miR-34a in AS-associated endothelial cell apoptosis are far from being addressed. Apolipoprotein E-deficient (ApoE
−/−
) mice fed with high-fat diet (HFD) were used as in vivo model of AS. Oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) were applied as in vitro model of AS. The effects of miR-34a on atherosclerotic lesions were evaluated by hematoxylin–eosin (HE) and Oil Red O staining. Pecam-1
+
endothelial cells were isolated from the aortic arch with flow cytometry. qRT-PCR and western blot were employed to measure gene and protein expression. The effects of miR-34a on cell viability, cell cycle distribution, and apoptosis were assessed by Cell counting kit (CCK)-8 and flow cytometry analysis. The relationship between miR-34a and Bcl-2 was confirmed by online softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP). miR-34a was upregulated in HFD-induced ApoE
−/−
mice and ox-LDL-treated HAECs. Anti-miR-34a decreased atherosclerotic lesions and inhibited Pecam-1
+
endothelial cells apoptosis in HFD-induced ApoE
−/−
mice. Moreover, anti-miR-34a significantly promoted cell viability, alleviated cell cycle arrest, and restrained apoptosis in ox-LDL-treated HAECs. Furthermore, Bcl-2 was identified as a target of miR-34a, and miR-34a inhibited Bcl-2 expression via binding to its 3′UTR. Rescue experiments demonstrated that Bcl-2 overexpression dramatically reversed miR-34a-mediated inhibition of cell growth and promotion of apoptosis in ox-LDL-exposed HAECs. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>29704100</pmid><doi>10.1007/s00380-018-1169-6</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4240-4586</orcidid></addata></record> |
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subjects | 3' Untranslated regions Aortic arch Apolipoprotein E Apoptosis Arteriosclerosis Atherosclerosis Bcl-2 protein Biomedical Engineering and Bioengineering Cardiac Surgery Cardiology CD31 antigen Cell cycle Cell growth Cholecystokinin Cytometry Endothelial cells Flow cytometry Gene expression High fat diet Immunoprecipitation Lesions Low density lipoprotein Medicine Medicine & Public Health Mice Oils & fats Original Article Ribonucleic acid RNA Target recognition Vascular Surgery |
title | Downregulation of miR-34a promotes endothelial cell growth and suppresses apoptosis in atherosclerosis by regulating Bcl-2 |
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