LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs
Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-12, Vol.24 (24), p.14231-14246 |
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| creator | Du, Jiao Han, Ruijuan Li, Yihua Liu, Xiaolin Liu, Shurong Cai, Zhenyu Xu, Zhaolong Li, Ya Yuan, Xuchun Guo, Xiuhai Lu, Bin Sun, Kai |
| description | Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose‐induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular‐related RNA‐binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA‐binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR‐26b‐5p, and QKI5 was speculated as the target of miR‐26b‐5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR‐26b‐5p/QKI‐5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As. |
| doi_str_mv | 10.1111/jcmm.16040 |
| format | Article |
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Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose‐induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular‐related RNA‐binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA‐binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR‐26b‐5p, and QKI5 was speculated as the target of miR‐26b‐5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR‐26b‐5p/QKI‐5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.16040</identifier><identifier>PMID: 33128346</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Aged ; Angina pectoris ; Angiogenesis ; Arteriosclerosis ; Atherosclerosis ; Binding sites ; Bioinformatics ; Biomarkers ; Blood vessels ; Calcification ; Cell Line, Tumor ; Cell proliferation ; Cells, Cultured ; Cholesterol ; Diabetic retinopathy ; Disease ; Endothelial cells ; Feedback ; Female ; Gene expression ; Gene Expression Regulation ; Genes, Reporter ; Glucose ; Glucose - metabolism ; Glucose - pharmacology ; Growth factors ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Hybridization ; Immunoprecipitation ; Kinases ; lncRNA HCG11 ; Male ; Medical imaging ; Medical prognosis ; MicroRNAs - genetics ; Middle Aged ; miR‐26b‐5p ; Neovascularization, Physiologic - genetics ; Non-coding RNA ; Original ; Patients ; Plaques ; Proteins ; QKI‐5 ; Ribonucleic acid ; RNA ; RNA Interference ; RNA, Long Noncoding - genetics ; RNA-binding protein ; RNA-Binding Proteins - genetics ; Vascularization</subject><ispartof>Journal of cellular and molecular medicine, 2020-12, Vol.24 (24), p.14231-14246</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4760-ba7d3dfb36dbf855800545aa04e707b591f001327d7e04fc38ca1f477765d9993</citedby><cites>FETCH-LOGICAL-c4760-ba7d3dfb36dbf855800545aa04e707b591f001327d7e04fc38ca1f477765d9993</cites><orcidid>0000-0003-4135-7412</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7753996/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7753996/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33128346$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Jiao</creatorcontrib><creatorcontrib>Han, Ruijuan</creatorcontrib><creatorcontrib>Li, Yihua</creatorcontrib><creatorcontrib>Liu, Xiaolin</creatorcontrib><creatorcontrib>Liu, Shurong</creatorcontrib><creatorcontrib>Cai, Zhenyu</creatorcontrib><creatorcontrib>Xu, Zhaolong</creatorcontrib><creatorcontrib>Li, Ya</creatorcontrib><creatorcontrib>Yuan, Xuchun</creatorcontrib><creatorcontrib>Guo, Xiuhai</creatorcontrib><creatorcontrib>Lu, Bin</creatorcontrib><creatorcontrib>Sun, Kai</creatorcontrib><title>LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose‐induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular‐related RNA‐binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA‐binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR‐26b‐5p, and QKI5 was speculated as the target of miR‐26b‐5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR‐26b‐5p/QKI‐5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.</description><subject>Aged</subject><subject>Angina pectoris</subject><subject>Angiogenesis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Biomarkers</subject><subject>Blood vessels</subject><subject>Calcification</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cells, Cultured</subject><subject>Cholesterol</subject><subject>Diabetic retinopathy</subject><subject>Disease</subject><subject>Endothelial cells</subject><subject>Feedback</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose - pharmacology</subject><subject>Growth factors</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Hybridization</subject><subject>Immunoprecipitation</subject><subject>Kinases</subject><subject>lncRNA HCG11</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Medical prognosis</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miR‐26b‐5p</subject><subject>Neovascularization, Physiologic - genetics</subject><subject>Non-coding RNA</subject><subject>Original</subject><subject>Patients</subject><subject>Plaques</subject><subject>Proteins</subject><subject>QKI‐5</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA-binding protein</subject><subject>RNA-Binding Proteins - genetics</subject><subject>Vascularization</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kt1qFDEUgAdRbK3e-AAy4I0I2yaTv8mNUIbard0qFuttyORnNutMMk12Kr0Tn8Bn9ElMu9uiXjSQnJDz8SWHnKJ4CcE-zONgpYZhH1KAwaNiF5K6mmGO8OPtHtao3imepbQCAFGI-NNiByFY1QjT3eLnwqvzj4flvDnOpsGd__7xq6JtXsl48Pn0hJTWGN1K9a3sQxjLaK5MTEaXS9cty66fVEgm087rSeXjMYbeWRPl2gVfSq_z7FzojDfJpdL5pWvdbS7Ycn7x9ahJz4snVvbJvNjGveLi_dGXZj5bfDo-aQ4XM4UZBbNWMo20bRHVra0JqQEgmEgJsGGAtYRDCwBEFdPMAGwVqpWEFjPGKNGcc7RXvNt4x6kdjFbGr6PsxRjdIOO1CNKJfzPeLUUXrgRjBHFOs-DNVhDD5WTSWgwuKdP30pswJVFhQjEEhIOMvv4PXYUp-lyeQIADSCmgD1IVpoxxnm_O1NsNpWJIKRp7_2QIxE0DiJsGELcNkOFXfxd5j979eAbgBvjuenP9gEp8aM7ONtI_hie8yQ</recordid><startdate>202012</startdate><enddate>202012</enddate><creator>Du, Jiao</creator><creator>Han, Ruijuan</creator><creator>Li, Yihua</creator><creator>Liu, Xiaolin</creator><creator>Liu, Shurong</creator><creator>Cai, Zhenyu</creator><creator>Xu, Zhaolong</creator><creator>Li, Ya</creator><creator>Yuan, Xuchun</creator><creator>Guo, Xiuhai</creator><creator>Lu, Bin</creator><creator>Sun, Kai</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4135-7412</orcidid></search><sort><creationdate>202012</creationdate><title>LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs</title><author>Du, Jiao ; Han, Ruijuan ; Li, Yihua ; Liu, Xiaolin ; Liu, Shurong ; Cai, Zhenyu ; Xu, Zhaolong ; Li, Ya ; Yuan, Xuchun ; Guo, Xiuhai ; Lu, Bin ; Sun, Kai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4760-ba7d3dfb36dbf855800545aa04e707b591f001327d7e04fc38ca1f477765d9993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Angina pectoris</topic><topic>Angiogenesis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Binding sites</topic><topic>Bioinformatics</topic><topic>Biomarkers</topic><topic>Blood vessels</topic><topic>Calcification</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cells, Cultured</topic><topic>Cholesterol</topic><topic>Diabetic retinopathy</topic><topic>Disease</topic><topic>Endothelial cells</topic><topic>Feedback</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose - pharmacology</topic><topic>Growth factors</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Hybridization</topic><topic>Immunoprecipitation</topic><topic>Kinases</topic><topic>lncRNA HCG11</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Medical prognosis</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miR‐26b‐5p</topic><topic>Neovascularization, Physiologic - genetics</topic><topic>Non-coding RNA</topic><topic>Original</topic><topic>Patients</topic><topic>Plaques</topic><topic>Proteins</topic><topic>QKI‐5</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA Interference</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA-binding protein</topic><topic>RNA-Binding Proteins - genetics</topic><topic>Vascularization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Jiao</creatorcontrib><creatorcontrib>Han, Ruijuan</creatorcontrib><creatorcontrib>Li, Yihua</creatorcontrib><creatorcontrib>Liu, Xiaolin</creatorcontrib><creatorcontrib>Liu, Shurong</creatorcontrib><creatorcontrib>Cai, Zhenyu</creatorcontrib><creatorcontrib>Xu, Zhaolong</creatorcontrib><creatorcontrib>Li, Ya</creatorcontrib><creatorcontrib>Yuan, Xuchun</creatorcontrib><creatorcontrib>Guo, Xiuhai</creatorcontrib><creatorcontrib>Lu, Bin</creatorcontrib><creatorcontrib>Sun, Kai</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Jiao</au><au>Han, Ruijuan</au><au>Li, Yihua</au><au>Liu, Xiaolin</au><au>Liu, Shurong</au><au>Cai, Zhenyu</au><au>Xu, Zhaolong</au><au>Li, Ya</au><au>Yuan, Xuchun</au><au>Guo, Xiuhai</au><au>Lu, Bin</au><au>Sun, Kai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-12</date><risdate>2020</risdate><volume>24</volume><issue>24</issue><spage>14231</spage><epage>14246</epage><pages>14231-14246</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose‐induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular‐related RNA‐binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA‐binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR‐26b‐5p, and QKI5 was speculated as the target of miR‐26b‐5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR‐26b‐5p/QKI‐5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>33128346</pmid><doi>10.1111/jcmm.16040</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-4135-7412</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Angina pectoris Angiogenesis Arteriosclerosis Atherosclerosis Binding sites Bioinformatics Biomarkers Blood vessels Calcification Cell Line, Tumor Cell proliferation Cells, Cultured Cholesterol Diabetic retinopathy Disease Endothelial cells Feedback Female Gene expression Gene Expression Regulation Genes, Reporter Glucose Glucose - metabolism Glucose - pharmacology Growth factors Human Umbilical Vein Endothelial Cells - metabolism Humans Hybridization Immunoprecipitation Kinases lncRNA HCG11 Male Medical imaging Medical prognosis MicroRNAs - genetics Middle Aged miR‐26b‐5p Neovascularization, Physiologic - genetics Non-coding RNA Original Patients Plaques Proteins QKI‐5 Ribonucleic acid RNA RNA Interference RNA, Long Noncoding - genetics RNA-binding protein RNA-Binding Proteins - genetics Vascularization |
| title | LncRNA HCG11/miR‐26b‐5p/QKI5 feedback loop reversed high glucose‐induced proliferation and angiogenesis inhibition of HUVECs |
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