MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice
Abdominal aortic aneurysm (AAA) is a potential lethal disease that is defined by an irreversible dilatation (>50%) of the aorta. During AAA expansion, the aortic wall is often remodeled, which is featured by extracellular matrix (ECM) degeneration, medial and adventitial inflammation, depletion a...
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description | Abdominal aortic aneurysm (AAA) is a potential lethal disease that is defined by an irreversible dilatation (>50%) of the aorta. During AAA expansion, the aortic wall is often remodeled, which is featured by extracellular matrix (ECM) degeneration, medial and adventitial inflammation, depletion and phenotypic switching of vascular smooth muscle cells (SMCs). Recent studies have suggested microRNAs as vital regulators for vascular SMC function. Our earlier work demonstrated an anti-AAA role of miR-126-5p in ApoE−/− mice infused with angiotensin (Ang) II. The present study aimed to further elucidate its role in AAA pathogenesis with a focus on aortic SMC phenotypic switching. Ventricular zone expressed PH domain containing 1 (VEPH1) was identified as a novel negative regulator for vascular SMC differentiation by our group, and its expression was negatively correlated to miR-126-5p in mouse abdominal aortas based on the present microarray data. In vivo, in addition attenuating Ang II infusion-induced aortic dilation and elastin degradation, miR-126-5p agomirs also significantly reduced the expression of VEPH1. In vitro, to induce synthetic transition of human aortic smooth muscle cells (hAoSMCs), cells were stimulated with 1 μM Ang II for 24 h. Ectopic overexpression of miR-126-5p restored the differentiation of hAoSMCs—the expression of contractile/differentiated SMC markers, MYH11, and α-SMA, increased, whilst that of synthetic/dedifferentiated SMC markers, PCNA and Vimentin, decreased. Both mus and homo VEPH1 genes were validated as direct targets for miR-126-5p. VEPH1 re-expression impaired miR-126-5p-induced differentiation of hAoSMCs. In addition, Ang II-induced upregulation in matrix metalloproteinase (MMP)-9 and MMP2, two key proteases responsible for ECM degradation, in mouse aortas and hAoSMCs was reduced by miR-126-5p overexpression as well. Collectively, these results reveal an important, but previously unexplored, role of miR-126-5p in inhibiting AAA development-associated aortic SMC dedifferentiation.
MiR-126-5p expression decreases abdominal aorta dilation in mice with Ang II-induced abdominal aortic aneurysm (AAA), and its agomirs limit experimental AAA formation. MiR-126-5p inhibits Ang II- and PDGF-BB-induced dedifferentiation of aortic smooth muscle cells (AoSMCs) in vitro. MiR-126-5p promotes contractile switching of AoSMCs exposed to Ang II by targeting VEPH1. |
doi_str_mv | 10.1038/s41374-020-0454-z |
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MiR-126-5p expression decreases abdominal aorta dilation in mice with Ang II-induced abdominal aortic aneurysm (AAA), and its agomirs limit experimental AAA formation. MiR-126-5p inhibits Ang II- and PDGF-BB-induced dedifferentiation of aortic smooth muscle cells (AoSMCs) in vitro. MiR-126-5p promotes contractile switching of AoSMCs exposed to Ang II by targeting VEPH1.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/s41374-020-0454-z</identifier><identifier>PMID: 32612287</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>13 ; 13/1 ; 13/109 ; 14 ; 14/34 ; 38 ; 38/1 ; 38/109 ; 42 ; 692/308/1426 ; 692/699/75/593/1287 ; Abdomen ; Aneurysms ; Angiotensin ; Angiotensin II ; Angiotensin II - metabolism ; Animals ; Aorta ; Aorta, Abdominal - cytology ; Aorta, Abdominal - metabolism ; Aortic Aneurysm, Abdominal - metabolism ; Aortic aneurysms ; Apolipoprotein E ; Biomarkers ; Cell Differentiation - genetics ; Cells, Cultured ; Coronary vessels ; Degeneration ; Degradation ; Depletion ; Differentiation ; Dilation ; Elastin ; Extracellular matrix ; Gelatinase A ; Laboratory Medicine ; Male ; Matrix metalloproteinase ; Matrix metalloproteinases ; Medicine ; Medicine & Public Health ; Metalloproteinase ; Mice ; Mice, Transgenic ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Muscle contraction ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - metabolism ; Muscles ; Nerve Tissue Proteins - metabolism ; Pathogenesis ; Pathology ; Platelet-derived growth factor ; Platelet-derived growth factor BB ; Proliferating cell nuclear antigen ; Regulators ; Smooth muscle ; Switching ; Ventricle ; Ventricular zone ; Vimentin</subject><ispartof>Laboratory investigation, 2020-12, Vol.100 (12), p.1564-1574</ispartof><rights>2020 United States & Canadian Academy of Pathology</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020</rights><rights>The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-49c6d10ff7c25ca475a3823a77aff324b1b4341ff3d5fdf9510403a3b16b96bf3</citedby><cites>FETCH-LOGICAL-c467t-49c6d10ff7c25ca475a3823a77aff324b1b4341ff3d5fdf9510403a3b16b96bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32612287$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Xiaofeng</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Pan, Yongquan</creatorcontrib><creatorcontrib>Li, Yongqi</creatorcontrib><creatorcontrib>Wang, Han</creatorcontrib><creatorcontrib>Pan, Shuang</creatorcontrib><creatorcontrib>Tian, Yu</creatorcontrib><creatorcontrib>Xu, Caiming</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><title>MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Abdominal aortic aneurysm (AAA) is a potential lethal disease that is defined by an irreversible dilatation (>50%) of the aorta. During AAA expansion, the aortic wall is often remodeled, which is featured by extracellular matrix (ECM) degeneration, medial and adventitial inflammation, depletion and phenotypic switching of vascular smooth muscle cells (SMCs). Recent studies have suggested microRNAs as vital regulators for vascular SMC function. Our earlier work demonstrated an anti-AAA role of miR-126-5p in ApoE−/− mice infused with angiotensin (Ang) II. The present study aimed to further elucidate its role in AAA pathogenesis with a focus on aortic SMC phenotypic switching. Ventricular zone expressed PH domain containing 1 (VEPH1) was identified as a novel negative regulator for vascular SMC differentiation by our group, and its expression was negatively correlated to miR-126-5p in mouse abdominal aortas based on the present microarray data. In vivo, in addition attenuating Ang II infusion-induced aortic dilation and elastin degradation, miR-126-5p agomirs also significantly reduced the expression of VEPH1. In vitro, to induce synthetic transition of human aortic smooth muscle cells (hAoSMCs), cells were stimulated with 1 μM Ang II for 24 h. Ectopic overexpression of miR-126-5p restored the differentiation of hAoSMCs—the expression of contractile/differentiated SMC markers, MYH11, and α-SMA, increased, whilst that of synthetic/dedifferentiated SMC markers, PCNA and Vimentin, decreased. Both mus and homo VEPH1 genes were validated as direct targets for miR-126-5p. VEPH1 re-expression impaired miR-126-5p-induced differentiation of hAoSMCs. In addition, Ang II-induced upregulation in matrix metalloproteinase (MMP)-9 and MMP2, two key proteases responsible for ECM degradation, in mouse aortas and hAoSMCs was reduced by miR-126-5p overexpression as well. Collectively, these results reveal an important, but previously unexplored, role of miR-126-5p in inhibiting AAA development-associated aortic SMC dedifferentiation.
MiR-126-5p expression decreases abdominal aorta dilation in mice with Ang II-induced abdominal aortic aneurysm (AAA), and its agomirs limit experimental AAA formation. MiR-126-5p inhibits Ang II- and PDGF-BB-induced dedifferentiation of aortic smooth muscle cells (AoSMCs) in vitro. MiR-126-5p promotes contractile switching of AoSMCs exposed to Ang II by targeting VEPH1.</description><subject>13</subject><subject>13/1</subject><subject>13/109</subject><subject>14</subject><subject>14/34</subject><subject>38</subject><subject>38/1</subject><subject>38/109</subject><subject>42</subject><subject>692/308/1426</subject><subject>692/699/75/593/1287</subject><subject>Abdomen</subject><subject>Aneurysms</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - metabolism</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta, Abdominal - cytology</subject><subject>Aorta, Abdominal - metabolism</subject><subject>Aortic Aneurysm, Abdominal - metabolism</subject><subject>Aortic aneurysms</subject><subject>Apolipoprotein E</subject><subject>Biomarkers</subject><subject>Cell Differentiation - genetics</subject><subject>Cells, Cultured</subject><subject>Coronary vessels</subject><subject>Degeneration</subject><subject>Degradation</subject><subject>Depletion</subject><subject>Differentiation</subject><subject>Dilation</subject><subject>Elastin</subject><subject>Extracellular matrix</subject><subject>Gelatinase A</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Muscle contraction</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscles</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Platelet-derived growth factor</subject><subject>Platelet-derived growth factor BB</subject><subject>Proliferating cell nuclear antigen</subject><subject>Regulators</subject><subject>Smooth muscle</subject><subject>Switching</subject><subject>Ventricle</subject><subject>Ventricular zone</subject><subject>Vimentin</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><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>eNp9kc9uFSEUxomxsdfqA7gxJG7c0PJvhrlx1TTV3qSNxqhbwjBwSzPAFZia20fxactkWpu46ArI-X3f4ZwPgHcEHxPMupPMCRMcYYoR5g1Hdy_AijSsvhgWL8EKY8pQ2zFxCF7nfIMx4bxtXoFDRltCaSdW4O-V-44IbVGzg7sUfSwmQx1DSUoXNxqY_7iir13Ywmihiqk4DbOPsVxDP2VdCW3GMcN-D4tKW1Nm9Nf5twsCVRigGkdz69TseloLmw1yYZi0qZV-iN4FNT66qmCmtM8eugC90-YNOLBqzObtw3kEfn4-_3F2gS6_ftmcnV4izVtREF_rdiDYWqFpoxUXjWIdZUoIZS2jvCc9Z5zU-9DYwa4bgjlmivWk7ddtb9kR-Lj41vl_TyYX6V2eh6ofilOWlJO1qIumXUU__IfexCnVGWZK1GYYi5kiC6VTzDkZK3fJeZX2kmA5ByeX4GQNTs7Bybuqef_gPPXeDP8Uj0lVgC5ArqWwNemp9XOunxaRqfu7dVWUtTOhrt8lo4scontGfQ-CVLfl</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Shi, Xiaofeng</creator><creator>Ma, Wei</creator><creator>Pan, Yongquan</creator><creator>Li, Yongqi</creator><creator>Wang, Han</creator><creator>Pan, Shuang</creator><creator>Tian, Yu</creator><creator>Xu, Caiming</creator><creator>Li, Lei</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20201201</creationdate><title>MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice</title><author>Shi, Xiaofeng ; Ma, Wei ; Pan, Yongquan ; Li, Yongqi ; Wang, Han ; Pan, Shuang ; Tian, Yu ; Xu, Caiming ; Li, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-49c6d10ff7c25ca475a3823a77aff324b1b4341ff3d5fdf9510403a3b16b96bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13</topic><topic>13/1</topic><topic>13/109</topic><topic>14</topic><topic>14/34</topic><topic>38</topic><topic>38/1</topic><topic>38/109</topic><topic>42</topic><topic>692/308/1426</topic><topic>692/699/75/593/1287</topic><topic>Abdomen</topic><topic>Aneurysms</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - metabolism</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta, Abdominal - cytology</topic><topic>Aorta, Abdominal - metabolism</topic><topic>Aortic Aneurysm, Abdominal - metabolism</topic><topic>Aortic aneurysms</topic><topic>Apolipoprotein E</topic><topic>Biomarkers</topic><topic>Cell Differentiation - genetics</topic><topic>Cells, Cultured</topic><topic>Coronary vessels</topic><topic>Degeneration</topic><topic>Degradation</topic><topic>Depletion</topic><topic>Differentiation</topic><topic>Dilation</topic><topic>Elastin</topic><topic>Extracellular matrix</topic><topic>Gelatinase A</topic><topic>Laboratory Medicine</topic><topic>Male</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Muscle contraction</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscles</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Platelet-derived growth factor</topic><topic>Platelet-derived growth factor BB</topic><topic>Proliferating cell nuclear antigen</topic><topic>Regulators</topic><topic>Smooth muscle</topic><topic>Switching</topic><topic>Ventricle</topic><topic>Ventricular zone</topic><topic>Vimentin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Xiaofeng</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Pan, Yongquan</creatorcontrib><creatorcontrib>Li, Yongqi</creatorcontrib><creatorcontrib>Wang, Han</creatorcontrib><creatorcontrib>Pan, Shuang</creatorcontrib><creatorcontrib>Tian, Yu</creatorcontrib><creatorcontrib>Xu, Caiming</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS 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>Public Health Database</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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Xiaofeng</au><au>Ma, Wei</au><au>Pan, Yongquan</au><au>Li, Yongqi</au><au>Wang, Han</au><au>Pan, Shuang</au><au>Tian, Yu</au><au>Xu, Caiming</au><au>Li, Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>100</volume><issue>12</issue><spage>1564</spage><epage>1574</epage><pages>1564-1574</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><abstract>Abdominal aortic aneurysm (AAA) is a potential lethal disease that is defined by an irreversible dilatation (>50%) of the aorta. During AAA expansion, the aortic wall is often remodeled, which is featured by extracellular matrix (ECM) degeneration, medial and adventitial inflammation, depletion and phenotypic switching of vascular smooth muscle cells (SMCs). Recent studies have suggested microRNAs as vital regulators for vascular SMC function. Our earlier work demonstrated an anti-AAA role of miR-126-5p in ApoE−/− mice infused with angiotensin (Ang) II. The present study aimed to further elucidate its role in AAA pathogenesis with a focus on aortic SMC phenotypic switching. Ventricular zone expressed PH domain containing 1 (VEPH1) was identified as a novel negative regulator for vascular SMC differentiation by our group, and its expression was negatively correlated to miR-126-5p in mouse abdominal aortas based on the present microarray data. In vivo, in addition attenuating Ang II infusion-induced aortic dilation and elastin degradation, miR-126-5p agomirs also significantly reduced the expression of VEPH1. In vitro, to induce synthetic transition of human aortic smooth muscle cells (hAoSMCs), cells were stimulated with 1 μM Ang II for 24 h. Ectopic overexpression of miR-126-5p restored the differentiation of hAoSMCs—the expression of contractile/differentiated SMC markers, MYH11, and α-SMA, increased, whilst that of synthetic/dedifferentiated SMC markers, PCNA and Vimentin, decreased. Both mus and homo VEPH1 genes were validated as direct targets for miR-126-5p. VEPH1 re-expression impaired miR-126-5p-induced differentiation of hAoSMCs. In addition, Ang II-induced upregulation in matrix metalloproteinase (MMP)-9 and MMP2, two key proteases responsible for ECM degradation, in mouse aortas and hAoSMCs was reduced by miR-126-5p overexpression as well. Collectively, these results reveal an important, but previously unexplored, role of miR-126-5p in inhibiting AAA development-associated aortic SMC dedifferentiation.
MiR-126-5p expression decreases abdominal aorta dilation in mice with Ang II-induced abdominal aortic aneurysm (AAA), and its agomirs limit experimental AAA formation. MiR-126-5p inhibits Ang II- and PDGF-BB-induced dedifferentiation of aortic smooth muscle cells (AoSMCs) in vitro. MiR-126-5p promotes contractile switching of AoSMCs exposed to Ang II by targeting VEPH1.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>32612287</pmid><doi>10.1038/s41374-020-0454-z</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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recordid | cdi_proquest_miscellaneous_2419713728 |
source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | 13 13/1 13/109 14 14/34 38 38/1 38/109 42 692/308/1426 692/699/75/593/1287 Abdomen Aneurysms Angiotensin Angiotensin II Angiotensin II - metabolism Animals Aorta Aorta, Abdominal - cytology Aorta, Abdominal - metabolism Aortic Aneurysm, Abdominal - metabolism Aortic aneurysms Apolipoprotein E Biomarkers Cell Differentiation - genetics Cells, Cultured Coronary vessels Degeneration Degradation Depletion Differentiation Dilation Elastin Extracellular matrix Gelatinase A Laboratory Medicine Male Matrix metalloproteinase Matrix metalloproteinases Medicine Medicine & Public Health Metalloproteinase Mice Mice, Transgenic MicroRNAs - genetics MicroRNAs - metabolism miRNA Muscle contraction Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - metabolism Muscles Nerve Tissue Proteins - metabolism Pathogenesis Pathology Platelet-derived growth factor Platelet-derived growth factor BB Proliferating cell nuclear antigen Regulators Smooth muscle Switching Ventricle Ventricular zone Vimentin |
title | MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T17%3A25%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MiR-126-5p%20promotes%20contractile%20switching%20of%20aortic%20smooth%20muscle%20cells%20by%20targeting%20VEPH1%20and%20alleviates%20Ang%20II-induced%20abdominal%20aortic%20aneurysm%20in%20mice&rft.jtitle=Laboratory%20investigation&rft.au=Shi,%20Xiaofeng&rft.date=2020-12-01&rft.volume=100&rft.issue=12&rft.spage=1564&rft.epage=1574&rft.pages=1564-1574&rft.issn=0023-6837&rft.eissn=1530-0307&rft_id=info:doi/10.1038/s41374-020-0454-z&rft_dat=%3Cproquest_cross%3E2473240078%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2473240078&rft_id=info:pmid/32612287&rft_els_id=S0023683722003336&rfr_iscdi=true |