Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction
Bone marrow-mesenchymal stem cell (BM-MSC) therapy improves the recovery of cardiac function after myocardial infarction (MI); however, the underlying molecular mechanisms are not completely understood. Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular...
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| creator | Song, Yi-Sun Joo, Hyun-Woo Park, In-Hwa Shen, Guang-Yin Lee, Yonggu Shin, Jeong Hun Kim, Hyuck Kim, Kyung-Soo |
| description | Bone marrow-mesenchymal stem cell (BM-MSC) therapy improves the recovery of cardiac function after myocardial infarction (MI); however, the underlying molecular mechanisms are not completely understood. Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular diseases. Here, we investigated the mechanisms underlying the effects of BM-MSC-derived paracrine factors and cardiac miRNAs on myocardial regeneration after MI. In our study, MI was induced by permanent ligation of the left anterior descending (LAD) coronary artery. BM-MSCs transplanted in infarcted rats significantly downregulated the expression of miRNA-23a and miRNA-92a and inhibited apoptosis in the myocardium. An in vitro experiment showed that supernatant from BM-MSCs cultured under hypoxia contained higher levels of vascular endothelial growth factor (VEGF) than that from BM-MSCs under normoxia. In addition, inhibition of miRNA-23a and miRNA-92a reduced cardiac apoptosis. Moreover, the VEGF-containing BM-MSC supernatant inhibited miRNA-23a and miRNA-92a expression and reduced apoptotic signaling in cardiomyocytes under hypoxia. These effects were inhibited when the supernatant was treated with neutralizing antibodies against VEGF. Our results indicate that the paracrine factor, VEGF, derived from transplanted BM-MSCs, regulated the expression of miRNAs such as miRNA-23a and miRNA-92a and exerted anti-apoptotic effects in cardiomyocytes after MI. |
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Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular diseases. Here, we investigated the mechanisms underlying the effects of BM-MSC-derived paracrine factors and cardiac miRNAs on myocardial regeneration after MI. In our study, MI was induced by permanent ligation of the left anterior descending (LAD) coronary artery. BM-MSCs transplanted in infarcted rats significantly downregulated the expression of miRNA-23a and miRNA-92a and inhibited apoptosis in the myocardium. An in vitro experiment showed that supernatant from BM-MSCs cultured under hypoxia contained higher levels of vascular endothelial growth factor (VEGF) than that from BM-MSCs under normoxia. In addition, inhibition of miRNA-23a and miRNA-92a reduced cardiac apoptosis. Moreover, the VEGF-containing BM-MSC supernatant inhibited miRNA-23a and miRNA-92a expression and reduced apoptotic signaling in cardiomyocytes under hypoxia. These effects were inhibited when the supernatant was treated with neutralizing antibodies against VEGF. Our results indicate that the paracrine factor, VEGF, derived from transplanted BM-MSCs, regulated the expression of miRNAs such as miRNA-23a and miRNA-92a and exerted anti-apoptotic effects in cardiomyocytes after MI.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0179972</identifier><identifier>PMID: 28662151</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antibodies ; Apoptosis ; Apoptosis - physiology ; Attenuation ; Biology and life sciences ; Bone marrow ; Bone Marrow Cells - cytology ; Bone Marrow Cells - metabolism ; Cardiology ; Cardiomyocytes ; Cardiovascular diseases ; Care and treatment ; Cells, Cultured ; Coronary artery ; Culture Media, Conditioned ; Disease Models, Animal ; Diseases ; Engineering ; Genetic aspects ; Heart ; Heart attack ; Heart attacks ; Heart diseases ; Heart failure ; Hypoxia ; In vitro methods and tests ; Infarction ; Inhibition ; Internal medicine ; Medicine ; Medicine and Health Sciences ; Mesenchymal stem cells ; Mesenchymal Stromal Cells - cytology ; Mesenchymal Stromal Cells - metabolism ; Mesenchyme ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - physiology ; miRNA ; Molecular modelling ; Myocardial infarction ; Myocardial Infarction - genetics ; Myocardial Infarction - pathology ; Myocardium ; Myocardium - metabolism ; Myocytes, Cardiac - metabolism ; Neutralizing ; Ostomy ; Paracrine signalling ; Penicillin ; Physiological aspects ; Physiology ; Rats ; Regeneration ; Regulation ; Research and Analysis Methods ; Rodents ; Science ; Stem cells ; Therapy ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - physiology</subject><ispartof>PloS one, 2017-06, Vol.12 (6), p.e0179972-e0179972</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Song 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 Song et al 2017 Song et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-4bf09823436df9e9c3b5cea4442a98fbbc1416a3d839093fd814df364112eff83</citedby><cites>FETCH-LOGICAL-c692t-4bf09823436df9e9c3b5cea4442a98fbbc1416a3d839093fd814df364112eff83</cites><orcidid>0000-0002-0891-1023</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/PMC5491110/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5491110/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28662151$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Fan, Guo-Chang</contributor><creatorcontrib>Song, Yi-Sun</creatorcontrib><creatorcontrib>Joo, Hyun-Woo</creatorcontrib><creatorcontrib>Park, In-Hwa</creatorcontrib><creatorcontrib>Shen, Guang-Yin</creatorcontrib><creatorcontrib>Lee, Yonggu</creatorcontrib><creatorcontrib>Shin, Jeong Hun</creatorcontrib><creatorcontrib>Kim, Hyuck</creatorcontrib><creatorcontrib>Kim, Kyung-Soo</creatorcontrib><title>Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Bone marrow-mesenchymal stem cell (BM-MSC) therapy improves the recovery of cardiac function after myocardial infarction (MI); however, the underlying molecular mechanisms are not completely understood. Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular diseases. Here, we investigated the mechanisms underlying the effects of BM-MSC-derived paracrine factors and cardiac miRNAs on myocardial regeneration after MI. In our study, MI was induced by permanent ligation of the left anterior descending (LAD) coronary artery. BM-MSCs transplanted in infarcted rats significantly downregulated the expression of miRNA-23a and miRNA-92a and inhibited apoptosis in the myocardium. An in vitro experiment showed that supernatant from BM-MSCs cultured under hypoxia contained higher levels of vascular endothelial growth factor (VEGF) than that from BM-MSCs under normoxia. In addition, inhibition of miRNA-23a and miRNA-92a reduced cardiac apoptosis. Moreover, the VEGF-containing BM-MSC supernatant inhibited miRNA-23a and miRNA-92a expression and reduced apoptotic signaling in cardiomyocytes under hypoxia. These effects were inhibited when the supernatant was treated with neutralizing antibodies against VEGF. Our results indicate that the paracrine factor, VEGF, derived from transplanted BM-MSCs, regulated the expression of miRNAs such as miRNA-23a and miRNA-92a and exerted anti-apoptotic effects in cardiomyocytes after MI.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Attenuation</subject><subject>Biology and life sciences</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular diseases</subject><subject>Care and treatment</subject><subject>Cells, Cultured</subject><subject>Coronary artery</subject><subject>Culture Media, Conditioned</subject><subject>Disease Models, Animal</subject><subject>Diseases</subject><subject>Engineering</subject><subject>Genetic aspects</subject><subject>Heart</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Hypoxia</subject><subject>In vitro methods and tests</subject><subject>Infarction</subject><subject>Inhibition</subject><subject>Internal medicine</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mesenchyme</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - physiology</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardium</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Neutralizing</subject><subject>Ostomy</subject><subject>Paracrine signalling</subject><subject>Penicillin</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Rats</subject><subject>Regeneration</subject><subject>Regulation</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Science</subject><subject>Stem cells</subject><subject>Therapy</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - physiology</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>DOA</sourceid><recordid>eNqNk81u1DAUhSMEolB4AwSWkBAsZohjJxNvkErFT6WKSuVna93Y1zOunHiwnYE-Hy-G05lWHdQFysKJ_Z1z42PfonhGyzllC_r2wo9hADdf-wHnJV0IsajuFY-oYNWsqUp2_9b7QfE4xouyrFnbNA-LgyoPFa3po-LP-ywnPYTgf5EeIw5qddmDIzFhTxQ6N9MY7AY12UBUo4NAcNA-rdDZjC2zLq2IAZV8IJASDiMkjERB0BYUgbVfJx9tJBsLJOAyWyTrB-LNDdPb8y9Hs4oBgUHvvkQFxA4kSyCR3mt0k6K_9FuRy4sGgpqsnhQPDLiIT3fjYfH944dvx59np2efTo6PTmeqEVWa8c6Uoq0YZ402AoViXa0QOOcViNZ0naKcNsB0y0QpmNEt5dqwhlNaoTEtOyxebH3Xzke5yz9KKihvq0UjmkycbAnt4UKug83BXkoPVl5N-LCUEJJVDmU2b5pOd9TULFcA0B10NVatKrko88kdFu921cauR61wSAHcnun-ymBXcuk3suaCUlpmg9c7g-B_jhiT7G2cThQG9OPVf-fSgnOa0Zf_oHfvbkctIW8g5-9zXTWZyiMuFqwtazqlNL-Dyo_G3qp824zN83uCN3uCzCT8nZYwxihPvp7_P3v2Y599dYtdIbi0it6N05WJ-yDfgir4GAOam5BpKadeu05DTr0md72WZc9vH9CN6Lq52F97PCck</recordid><startdate>20170629</startdate><enddate>20170629</enddate><creator>Song, Yi-Sun</creator><creator>Joo, Hyun-Woo</creator><creator>Park, In-Hwa</creator><creator>Shen, Guang-Yin</creator><creator>Lee, Yonggu</creator><creator>Shin, Jeong Hun</creator><creator>Kim, Hyuck</creator><creator>Kim, Kyung-Soo</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>AEUYN</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>DOA</scope><orcidid>https://orcid.org/0000-0002-0891-1023</orcidid></search><sort><creationdate>20170629</creationdate><title>Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction</title><author>Song, Yi-Sun ; Joo, Hyun-Woo ; Park, In-Hwa ; Shen, Guang-Yin ; Lee, Yonggu ; Shin, Jeong Hun ; Kim, Hyuck ; Kim, Kyung-Soo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-4bf09823436df9e9c3b5cea4442a98fbbc1416a3d839093fd814df364112eff83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Apoptosis - 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Academic</collection><collection>PubMed Central (Full Participant titles)</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>Song, Yi-Sun</au><au>Joo, Hyun-Woo</au><au>Park, In-Hwa</au><au>Shen, Guang-Yin</au><au>Lee, Yonggu</au><au>Shin, Jeong Hun</au><au>Kim, Hyuck</au><au>Kim, Kyung-Soo</au><au>Fan, Guo-Chang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-06-29</date><risdate>2017</risdate><volume>12</volume><issue>6</issue><spage>e0179972</spage><epage>e0179972</epage><pages>e0179972-e0179972</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Bone marrow-mesenchymal stem cell (BM-MSC) therapy improves the recovery of cardiac function after myocardial infarction (MI); however, the underlying molecular mechanisms are not completely understood. Recent studies have shown that microRNAs (miRNAs) modulate the pathophysiology of cardiovascular diseases. Here, we investigated the mechanisms underlying the effects of BM-MSC-derived paracrine factors and cardiac miRNAs on myocardial regeneration after MI. In our study, MI was induced by permanent ligation of the left anterior descending (LAD) coronary artery. BM-MSCs transplanted in infarcted rats significantly downregulated the expression of miRNA-23a and miRNA-92a and inhibited apoptosis in the myocardium. An in vitro experiment showed that supernatant from BM-MSCs cultured under hypoxia contained higher levels of vascular endothelial growth factor (VEGF) than that from BM-MSCs under normoxia. In addition, inhibition of miRNA-23a and miRNA-92a reduced cardiac apoptosis. Moreover, the VEGF-containing BM-MSC supernatant inhibited miRNA-23a and miRNA-92a expression and reduced apoptotic signaling in cardiomyocytes under hypoxia. These effects were inhibited when the supernatant was treated with neutralizing antibodies against VEGF. Our results indicate that the paracrine factor, VEGF, derived from transplanted BM-MSCs, regulated the expression of miRNAs such as miRNA-23a and miRNA-92a and exerted anti-apoptotic effects in cardiomyocytes after MI.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28662151</pmid><doi>10.1371/journal.pone.0179972</doi><tpages>e0179972</tpages><orcidid>https://orcid.org/0000-0002-0891-1023</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1914827696 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Antibodies Apoptosis Apoptosis - physiology Attenuation Biology and life sciences Bone marrow Bone Marrow Cells - cytology Bone Marrow Cells - metabolism Cardiology Cardiomyocytes Cardiovascular diseases Care and treatment Cells, Cultured Coronary artery Culture Media, Conditioned Disease Models, Animal Diseases Engineering Genetic aspects Heart Heart attack Heart attacks Heart diseases Heart failure Hypoxia In vitro methods and tests Infarction Inhibition Internal medicine Medicine Medicine and Health Sciences Mesenchymal stem cells Mesenchymal Stromal Cells - cytology Mesenchymal Stromal Cells - metabolism Mesenchyme MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - physiology miRNA Molecular modelling Myocardial infarction Myocardial Infarction - genetics Myocardial Infarction - pathology Myocardium Myocardium - metabolism Myocytes, Cardiac - metabolism Neutralizing Ostomy Paracrine signalling Penicillin Physiological aspects Physiology Rats Regeneration Regulation Research and Analysis Methods Rodents Science Stem cells Therapy Vascular endothelial growth factor Vascular Endothelial Growth Factor A - physiology |
| title | Bone marrow mesenchymal stem cell-derived vascular endothelial growth factor attenuates cardiac apoptosis via regulation of cardiac miRNA-23a and miRNA-92a in a rat model of myocardial infarction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T19%3A37%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Bone%20marrow%20mesenchymal%20stem%20cell-derived%20vascular%20endothelial%20growth%20factor%20attenuates%20cardiac%20apoptosis%20via%20regulation%20of%20cardiac%20miRNA-23a%20and%20miRNA-92a%20in%20a%20rat%20model%20of%20myocardial%20infarction&rft.jtitle=PloS%20one&rft.au=Song,%20Yi-Sun&rft.date=2017-06-29&rft.volume=12&rft.issue=6&rft.spage=e0179972&rft.epage=e0179972&rft.pages=e0179972-e0179972&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0179972&rft_dat=%3Cgale_plos_%3EA497380518%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1914827696&rft_id=info:pmid/28662151&rft_galeid=A497380518&rft_doaj_id=oai_doaj_org_article_81466bdb1f53411aadbab5e28c049019&rfr_iscdi=true |