Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle
Caveolae are membrane invaginations present at high densities in muscle and fat. Recent work has demonstrated that myocardin family coactivators (MYOCD, MKL1), which are important for contractile differentiation and cell motility, increase caveolin (CAV1, CAV2, CAV3) and cavin (CAVIN1, CAVIN2, CAVIN...
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description | Caveolae are membrane invaginations present at high densities in muscle and fat. Recent work has demonstrated that myocardin family coactivators (MYOCD, MKL1), which are important for contractile differentiation and cell motility, increase caveolin (CAV1, CAV2, CAV3) and cavin (CAVIN1, CAVIN2, CAVIN3) transcription, but several aspects of this control mechanism remain to be investigated. Here, using promoter reporter assays we found that both MKL1/MRTF-A and MKL2/MRTF-B control caveolins and cavins via their proximal promoter sequences. Silencing of MKL1 and MKL2 in smooth muscle cells moreover reduced CAV1 and CAVIN1 mRNA levels by well over 50%, as did treatment with second generation inhibitors of MKL activity. GATA6, which modulates expression of smooth muscle-specific genes, reduced CAV1 and CAV2, whereas the cavins were unaffected or increased. Viral overexpression of MKL1 and myocardin induced caveolin and cavin expression in bladder smooth muscle cells from rats and humans and MYOCD correlated tightly with CAV1 and CAVIN1 in human bladder specimens. A recently described activator of MKL-driven transcription (ISX) failed to induce CAV1/CAVIN1 which may be due to an unusual transactivation mechanism. In all, these findings further support the view that myocardin family coactivators are important transcriptional drivers of caveolins and cavins in smooth muscle. |
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Recent work has demonstrated that myocardin family coactivators (MYOCD, MKL1), which are important for contractile differentiation and cell motility, increase caveolin (CAV1, CAV2, CAV3) and cavin (CAVIN1, CAVIN2, CAVIN3) transcription, but several aspects of this control mechanism remain to be investigated. Here, using promoter reporter assays we found that both MKL1/MRTF-A and MKL2/MRTF-B control caveolins and cavins via their proximal promoter sequences. Silencing of MKL1 and MKL2 in smooth muscle cells moreover reduced CAV1 and CAVIN1 mRNA levels by well over 50%, as did treatment with second generation inhibitors of MKL activity. GATA6, which modulates expression of smooth muscle-specific genes, reduced CAV1 and CAV2, whereas the cavins were unaffected or increased. Viral overexpression of MKL1 and myocardin induced caveolin and cavin expression in bladder smooth muscle cells from rats and humans and MYOCD correlated tightly with CAV1 and CAVIN1 in human bladder specimens. A recently described activator of MKL-driven transcription (ISX) failed to induce CAV1/CAVIN1 which may be due to an unusual transactivation mechanism. In all, these findings further support the view that myocardin family coactivators are important transcriptional drivers of caveolins and cavins in smooth muscle.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0176759</identifier><identifier>PMID: 28542204</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetylcholine receptors (muscarinic) ; Actin ; Adipocytes ; Adipogenesis ; Air conditioning ; Animals ; Aorta ; Arteries ; Assaying ; Atmosphere ; Basic Medicine ; Biochemistry ; Biology and Life Sciences ; Biomechanics ; Biosynthesis ; Bladder ; Breast cancer ; Cancer ; Carbon dioxide ; Cardiac and Cardiovascular Systems ; Caveolins ; Caveolins - genetics ; Caveolins - metabolism ; Cell and Molecular Biology ; Cell culture ; Cell differentiation ; Cell- och molekylärbiologi ; Cells, Cultured ; Cholesterol ; Clinical Medicine ; Coronary vessels ; Deoxyribonucleic acid ; Differentiation (biology) ; Dissection ; DNA ; Dystrophy ; Evolution ; Female ; Gene expression ; Gene regulation ; Genetic aspects ; Genetic control ; Guidelines ; Heart diseases ; Homeostasis ; Hypoxia ; Inhibition ; Inhibitors ; Kardiologi ; Klinisk medicin ; Male ; Medical and Health Sciences ; Medical science ; Medicin och hälsovetenskap ; Medicine and Health Sciences ; Medicinska och farmaceutiska grundvetenskaper ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Metastases ; Mice ; Mice, Inbred C57BL ; Movement disorders ; Muscle, Smooth - metabolism ; Muscles ; Muscular dystrophy ; Mutation ; Myocytes, Smooth Muscle - metabolism ; Neurodegenerative diseases ; Nuclear Proteins - metabolism ; Optimization ; Organelles ; Parkinson's disease ; Pharmacology ; Physiological aspects ; Pipes ; Promoter Regions, Genetic - genetics ; Promoters (Genetics) ; Prostate cancer ; Proteins ; Rats ; Rats, Sprague-Dawley ; Regeneration (physiology) ; Regulatory mechanisms (biology) ; Rodents ; Science ; Smooth muscle ; Stem cells ; Stimulation ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription factors ; Transcription, Genetic - genetics ; Transcriptional Activation - genetics ; Urinary bladder ; Urinary Bladder - metabolism ; Urologi och njurmedicin ; Urology ; Urology and Nephrology ; Veins & arteries ; Wound healing</subject><ispartof>PloS one, 2017-05, Vol.12 (5), p.e0176759-e0176759</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Zhu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Zhu et al 2017 Zhu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c761t-17f4779c7636fbda6891fb95ab7d401217cdb85e5389573621c06f0ad366c8143</citedby><cites>FETCH-LOGICAL-c761t-17f4779c7636fbda6891fb95ab7d401217cdb85e5389573621c06f0ad366c8143</cites><orcidid>0000-0002-7255-5510</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/PMC5444588/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5444588/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,552,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28542204$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/fe21adfe-799d-439a-bb68-2468c5518f95$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Nabi, Ivan R</contributor><creatorcontrib>Zhu, Baoyi</creatorcontrib><creatorcontrib>Rippe, Catarina</creatorcontrib><creatorcontrib>Thi Hien, Tran</creatorcontrib><creatorcontrib>Zeng, Jianwen</creatorcontrib><creatorcontrib>Albinsson, Sebastian</creatorcontrib><creatorcontrib>Stenkula, Karin G</creatorcontrib><creatorcontrib>Uvelius, Bengt</creatorcontrib><creatorcontrib>Swärd, Karl</creatorcontrib><title>Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Caveolae are membrane invaginations present at high densities in muscle and fat. Recent work has demonstrated that myocardin family coactivators (MYOCD, MKL1), which are important for contractile differentiation and cell motility, increase caveolin (CAV1, CAV2, CAV3) and cavin (CAVIN1, CAVIN2, CAVIN3) transcription, but several aspects of this control mechanism remain to be investigated. Here, using promoter reporter assays we found that both MKL1/MRTF-A and MKL2/MRTF-B control caveolins and cavins via their proximal promoter sequences. Silencing of MKL1 and MKL2 in smooth muscle cells moreover reduced CAV1 and CAVIN1 mRNA levels by well over 50%, as did treatment with second generation inhibitors of MKL activity. GATA6, which modulates expression of smooth muscle-specific genes, reduced CAV1 and CAV2, whereas the cavins were unaffected or increased. Viral overexpression of MKL1 and myocardin induced caveolin and cavin expression in bladder smooth muscle cells from rats and humans and MYOCD correlated tightly with CAV1 and CAVIN1 in human bladder specimens. A recently described activator of MKL-driven transcription (ISX) failed to induce CAV1/CAVIN1 which may be due to an unusual transactivation mechanism. In all, these findings further support the view that myocardin family coactivators are important transcriptional drivers of caveolins and cavins in smooth muscle.</description><subject>Acetylcholine receptors (muscarinic)</subject><subject>Actin</subject><subject>Adipocytes</subject><subject>Adipogenesis</subject><subject>Air conditioning</subject><subject>Animals</subject><subject>Aorta</subject><subject>Arteries</subject><subject>Assaying</subject><subject>Atmosphere</subject><subject>Basic Medicine</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Biomechanics</subject><subject>Biosynthesis</subject><subject>Bladder</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Carbon dioxide</subject><subject>Cardiac and Cardiovascular Systems</subject><subject>Caveolins</subject><subject>Caveolins - genetics</subject><subject>Caveolins - metabolism</subject><subject>Cell and Molecular Biology</subject><subject>Cell culture</subject><subject>Cell differentiation</subject><subject>Cell- och molekylärbiologi</subject><subject>Cells, Cultured</subject><subject>Cholesterol</subject><subject>Clinical Medicine</subject><subject>Coronary vessels</subject><subject>Deoxyribonucleic acid</subject><subject>Differentiation (biology)</subject><subject>Dissection</subject><subject>DNA</subject><subject>Dystrophy</subject><subject>Evolution</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genetic aspects</subject><subject>Genetic control</subject><subject>Guidelines</subject><subject>Heart diseases</subject><subject>Homeostasis</subject><subject>Hypoxia</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Kardiologi</subject><subject>Klinisk medicin</subject><subject>Male</subject><subject>Medical and Health Sciences</subject><subject>Medical science</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicine and Health Sciences</subject><subject>Medicinska och farmaceutiska grundvetenskaper</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Movement disorders</subject><subject>Muscle, Smooth - metabolism</subject><subject>Muscles</subject><subject>Muscular dystrophy</subject><subject>Mutation</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Neurodegenerative diseases</subject><subject>Nuclear Proteins - metabolism</subject><subject>Optimization</subject><subject>Organelles</subject><subject>Parkinson's disease</subject><subject>Pharmacology</subject><subject>Physiological aspects</subject><subject>Pipes</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Promoters (Genetics)</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Regeneration (physiology)</subject><subject>Regulatory mechanisms (biology)</subject><subject>Rodents</subject><subject>Science</subject><subject>Smooth muscle</subject><subject>Stem cells</subject><subject>Stimulation</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription factors</subject><subject>Transcription, Genetic - genetics</subject><subject>Transcriptional Activation - genetics</subject><subject>Urinary bladder</subject><subject>Urinary Bladder - metabolism</subject><subject>Urologi och njurmedicin</subject><subject>Urology</subject><subject>Urology and Nephrology</subject><subject>Veins & arteries</subject><subject>Wound healing</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11rFDEUhgdRbK3-A9EBQfRi18l3ciOU4kehULDqbcjkYzclM9kmM9UFf7yZ7rZ0pBcyZJKcvOdJ8s6cqnoJmiVADHy4jGPqVVhuYm-XDWCUEfGoOgQCwQWFDXp8b3xQPcv5smkI4pQ-rQ4gJxjCBh9Wfy5854NKdbKrMaghpm3dWb1Wvc9drqOrtbq2Mfg-16o302watkW1jVol4_vaqYLY1joqPfjriZHrElZpsMmrcJPXBmWMTXXuYhzWdTdmHezz6olTIdsX-_6o-vH50_eTr4uz8y-nJ8dnC80oGBaAOcyYKBNEXWsU5QK4VhDVMoMbAAHTpuXEltsJwhCFQDfUNcogSjUHGB1Vr3fcTYhZ7o3LEogGYsaLc0VxulOYqC7lJvlOpa2MysubQEwrWa7jy5mlM4g4TctbQMyR4a1goLHcMMGshaiwznas_MtuxnZGC-OmtLY0mQvKQqCMs5IJYSRGQsm2pVxCTLkmBHAnSMF93B9-bDtrtO2HpMKMOl_p_Vqu4rUkGGPCeQG82wNSvBptHmTns7YhqN7G8cYGBKjAfNrrzT_Sh83aq1aq-OF7F8u-eoLKYywgh0CQyfTlA6ryGNt5XX5a50t8lvB-llA0g_09rNSYszy9-Pb_2vOfc-3be9q1VWFY5xjGwcc-z4V4J9Qp5pysuzMZNHKquVs35FRzcl9zJe3V_Q90l3RbZOgvrVgn8Q</recordid><startdate>20170525</startdate><enddate>20170525</enddate><creator>Zhu, Baoyi</creator><creator>Rippe, Catarina</creator><creator>Thi Hien, Tran</creator><creator>Zeng, Jianwen</creator><creator>Albinsson, Sebastian</creator><creator>Stenkula, Karin G</creator><creator>Uvelius, Bengt</creator><creator>Swärd, Karl</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AGCHP</scope><scope>AOWAS</scope><scope>D8T</scope><scope>D95</scope><scope>ZZAVC</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7255-5510</orcidid></search><sort><creationdate>20170525</creationdate><title>Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle</title><author>Zhu, Baoyi ; Rippe, Catarina ; Thi Hien, Tran ; Zeng, Jianwen ; Albinsson, Sebastian ; Stenkula, Karin G ; Uvelius, Bengt ; Swärd, Karl</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c761t-17f4779c7636fbda6891fb95ab7d401217cdb85e5389573621c06f0ad366c8143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acetylcholine receptors (muscarinic)</topic><topic>Actin</topic><topic>Adipocytes</topic><topic>Adipogenesis</topic><topic>Air conditioning</topic><topic>Animals</topic><topic>Aorta</topic><topic>Arteries</topic><topic>Assaying</topic><topic>Atmosphere</topic><topic>Basic Medicine</topic><topic>Biochemistry</topic><topic>Biology and Life Sciences</topic><topic>Biomechanics</topic><topic>Biosynthesis</topic><topic>Bladder</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Carbon dioxide</topic><topic>Cardiac and Cardiovascular Systems</topic><topic>Caveolins</topic><topic>Caveolins - genetics</topic><topic>Caveolins - metabolism</topic><topic>Cell and Molecular Biology</topic><topic>Cell culture</topic><topic>Cell differentiation</topic><topic>Cell- och molekylärbiologi</topic><topic>Cells, Cultured</topic><topic>Cholesterol</topic><topic>Clinical Medicine</topic><topic>Coronary vessels</topic><topic>Deoxyribonucleic acid</topic><topic>Differentiation (biology)</topic><topic>Dissection</topic><topic>DNA</topic><topic>Dystrophy</topic><topic>Evolution</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Genetic aspects</topic><topic>Genetic control</topic><topic>Guidelines</topic><topic>Heart diseases</topic><topic>Homeostasis</topic><topic>Hypoxia</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Kardiologi</topic><topic>Klinisk medicin</topic><topic>Male</topic><topic>Medical and Health Sciences</topic><topic>Medical science</topic><topic>Medicin och hälsovetenskap</topic><topic>Medicine and Health Sciences</topic><topic>Medicinska och farmaceutiska grundvetenskaper</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Movement disorders</topic><topic>Muscle, Smooth - metabolism</topic><topic>Muscles</topic><topic>Muscular dystrophy</topic><topic>Mutation</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Neurodegenerative diseases</topic><topic>Nuclear Proteins - metabolism</topic><topic>Optimization</topic><topic>Organelles</topic><topic>Parkinson's disease</topic><topic>Pharmacology</topic><topic>Physiological aspects</topic><topic>Pipes</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Promoters (Genetics)</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Regeneration (physiology)</topic><topic>Regulatory mechanisms (biology)</topic><topic>Rodents</topic><topic>Science</topic><topic>Smooth muscle</topic><topic>Stem cells</topic><topic>Stimulation</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription factors</topic><topic>Transcription, Genetic - genetics</topic><topic>Transcriptional Activation - genetics</topic><topic>Urinary bladder</topic><topic>Urinary Bladder - metabolism</topic><topic>Urologi och njurmedicin</topic><topic>Urology</topic><topic>Urology and Nephrology</topic><topic>Veins & arteries</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Baoyi</creatorcontrib><creatorcontrib>Rippe, Catarina</creatorcontrib><creatorcontrib>Thi Hien, Tran</creatorcontrib><creatorcontrib>Zeng, Jianwen</creatorcontrib><creatorcontrib>Albinsson, Sebastian</creatorcontrib><creatorcontrib>Stenkula, Karin G</creatorcontrib><creatorcontrib>Uvelius, Bengt</creatorcontrib><creatorcontrib>Swärd, Karl</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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 Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</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>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SWEPUB Lunds universitet full text</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Lunds universitet</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Baoyi</au><au>Rippe, Catarina</au><au>Thi Hien, Tran</au><au>Zeng, Jianwen</au><au>Albinsson, Sebastian</au><au>Stenkula, Karin G</au><au>Uvelius, Bengt</au><au>Swärd, Karl</au><au>Nabi, Ivan R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-05-25</date><risdate>2017</risdate><volume>12</volume><issue>5</issue><spage>e0176759</spage><epage>e0176759</epage><pages>e0176759-e0176759</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Caveolae are membrane invaginations present at high densities in muscle and fat. Recent work has demonstrated that myocardin family coactivators (MYOCD, MKL1), which are important for contractile differentiation and cell motility, increase caveolin (CAV1, CAV2, CAV3) and cavin (CAVIN1, CAVIN2, CAVIN3) transcription, but several aspects of this control mechanism remain to be investigated. Here, using promoter reporter assays we found that both MKL1/MRTF-A and MKL2/MRTF-B control caveolins and cavins via their proximal promoter sequences. Silencing of MKL1 and MKL2 in smooth muscle cells moreover reduced CAV1 and CAVIN1 mRNA levels by well over 50%, as did treatment with second generation inhibitors of MKL activity. GATA6, which modulates expression of smooth muscle-specific genes, reduced CAV1 and CAV2, whereas the cavins were unaffected or increased. Viral overexpression of MKL1 and myocardin induced caveolin and cavin expression in bladder smooth muscle cells from rats and humans and MYOCD correlated tightly with CAV1 and CAVIN1 in human bladder specimens. A recently described activator of MKL-driven transcription (ISX) failed to induce CAV1/CAVIN1 which may be due to an unusual transactivation mechanism. In all, these findings further support the view that myocardin family coactivators are important transcriptional drivers of caveolins and cavins in smooth muscle.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28542204</pmid><doi>10.1371/journal.pone.0176759</doi><tpages>e0176759</tpages><orcidid>https://orcid.org/0000-0002-7255-5510</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2017-05, Vol.12 (5), p.e0176759-e0176759 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1902478767 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SWEPUB Freely available online; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Acetylcholine receptors (muscarinic) Actin Adipocytes Adipogenesis Air conditioning Animals Aorta Arteries Assaying Atmosphere Basic Medicine Biochemistry Biology and Life Sciences Biomechanics Biosynthesis Bladder Breast cancer Cancer Carbon dioxide Cardiac and Cardiovascular Systems Caveolins Caveolins - genetics Caveolins - metabolism Cell and Molecular Biology Cell culture Cell differentiation Cell- och molekylärbiologi Cells, Cultured Cholesterol Clinical Medicine Coronary vessels Deoxyribonucleic acid Differentiation (biology) Dissection DNA Dystrophy Evolution Female Gene expression Gene regulation Genetic aspects Genetic control Guidelines Heart diseases Homeostasis Hypoxia Inhibition Inhibitors Kardiologi Klinisk medicin Male Medical and Health Sciences Medical science Medicin och hälsovetenskap Medicine and Health Sciences Medicinska och farmaceutiska grundvetenskaper Membrane Proteins - genetics Membrane Proteins - metabolism Metastases Mice Mice, Inbred C57BL Movement disorders Muscle, Smooth - metabolism Muscles Muscular dystrophy Mutation Myocytes, Smooth Muscle - metabolism Neurodegenerative diseases Nuclear Proteins - metabolism Optimization Organelles Parkinson's disease Pharmacology Physiological aspects Pipes Promoter Regions, Genetic - genetics Promoters (Genetics) Prostate cancer Proteins Rats Rats, Sprague-Dawley Regeneration (physiology) Regulatory mechanisms (biology) Rodents Science Smooth muscle Stem cells Stimulation Trans-Activators - genetics Trans-Activators - metabolism Transcription factors Transcription, Genetic - genetics Transcriptional Activation - genetics Urinary bladder Urinary Bladder - metabolism Urologi och njurmedicin Urology Urology and Nephrology Veins & arteries Wound healing |
title | Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle |
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