Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts
Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which...
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| description | Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which can antagonize TGF-β1 signaling. We hypothesized that TGF-β1-induced cardiac fibroblast to myofibroblast differentiation is abrogated by FGF-2 and ASC conditioned medium (ASC-CMed). Our experiments demonstrated that TGF-β1 treatment-induced cardiac fibroblast differentiation into myofibroblasts, as evidenced by the formation of contractile stress fibers rich in αSMA. FGF-2 blocked the differentiation, as evidenced by the reduction in gene (
TAGLN
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| doi_str_mv | 10.1038/s41598-018-34747-3 |
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TAGLN
, p < 0.0001;
ACTA2
, p = 0.0056) and protein (αSMA, p = 0.0338) expression of mesenchymal markers and extracellular matrix components gene expression (
COL1A1
, p < 0.0001;
COL3A1
, p = 0.0029). ASC-CMed did not block myofibroblast differentiation. The treatment with FGF-2 increased matrix metalloproteinases gene expression (
MMP1
, p < 0.0001;
MMP14
, p = 0.0027) and decreased the expression of tissue inhibitor of metalloproteinase gene
TIMP2
(p = 0.0023). ASC-CMed did not influence these genes. The proliferation of TGF-β1-induced human cardiac fibroblasts was restored by both FGF-2 (p = 0.0002) and ASC-CMed (p = 0.0121). The present study supports the anti-fibrotic effects of FGF-2 through the blockage of cardiac fibroblast differentiation into myofibroblasts. ASC-CMed, however, did not replicate the anti-fibrotic effects of FGF-2
in vitro
.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-34747-3</identifier><identifier>PMID: 30413733</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/100 ; 14 ; 14/1 ; 14/63 ; 38 ; 38/77 ; 38/90 ; 631/532/2118/2074 ; 692/4019/592/2725 ; 82/80 ; Adipose tissue ; Cell Differentiation - drug effects ; Cells, Cultured ; Collagen (type I) ; Culture Media, Conditioned - pharmacology ; Extracellular matrix ; Extracellular Matrix - metabolism ; Fibers ; Fibroblast growth factor 2 ; Fibroblast Growth Factor 2 - pharmacology ; Fibroblasts ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Gene expression ; Growth factors ; Heart ; Humanities and Social Sciences ; Humans ; Mesenchymal Stem Cells - cytology ; Mesenchymal Stem Cells - metabolism ; Mesenchyme ; Metalloproteinase ; multidisciplinary ; Muscle contraction ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myofibroblasts - cytology ; Myofibroblasts - drug effects ; Myofibroblasts - metabolism ; Science ; Science (multidisciplinary) ; Secretome ; Signal Transduction ; Stromal cells ; Tissue inhibitor of metalloproteinase 2 ; Transforming Growth Factor beta1 - pharmacology ; Transforming growth factor-b1</subject><ispartof>Scientific reports, 2018-11, Vol.8 (1), p.16633-10, Article 16633</ispartof><rights>The Author(s) 2018</rights><rights>2018. 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-c474t-8634433fa54330cf5550409e2db8f3be4aaf4be03a848ea9f91d044b25bb63fb3</citedby><cites>FETCH-LOGICAL-c474t-8634433fa54330cf5550409e2db8f3be4aaf4be03a848ea9f91d044b25bb63fb3</cites><orcidid>0000-0003-0179-4976 ; 0000-0002-7128-2741</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/PMC6226511/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6226511/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30413733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liguori, Tácia Tavares Aquinas</creatorcontrib><creatorcontrib>Liguori, Gabriel Romero</creatorcontrib><creatorcontrib>Moreira, Luiz Felipe Pinho</creatorcontrib><creatorcontrib>Harmsen, Martin Conrad</creatorcontrib><title>Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which can antagonize TGF-β1 signaling. We hypothesized that TGF-β1-induced cardiac fibroblast to myofibroblast differentiation is abrogated by FGF-2 and ASC conditioned medium (ASC-CMed). Our experiments demonstrated that TGF-β1 treatment-induced cardiac fibroblast differentiation into myofibroblasts, as evidenced by the formation of contractile stress fibers rich in αSMA. FGF-2 blocked the differentiation, as evidenced by the reduction in gene (
TAGLN
, p < 0.0001;
ACTA2
, p = 0.0056) and protein (αSMA, p = 0.0338) expression of mesenchymal markers and extracellular matrix components gene expression (
COL1A1
, p < 0.0001;
COL3A1
, p = 0.0029). ASC-CMed did not block myofibroblast differentiation. The treatment with FGF-2 increased matrix metalloproteinases gene expression (
MMP1
, p < 0.0001;
MMP14
, p = 0.0027) and decreased the expression of tissue inhibitor of metalloproteinase gene
TIMP2
(p = 0.0023). ASC-CMed did not influence these genes. The proliferation of TGF-β1-induced human cardiac fibroblasts was restored by both FGF-2 (p = 0.0002) and ASC-CMed (p = 0.0121). The present study supports the anti-fibrotic effects of FGF-2 through the blockage of cardiac fibroblast differentiation into myofibroblasts. ASC-CMed, however, did not replicate the anti-fibrotic effects of FGF-2
in vitro
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cytology</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Mesenchyme</subject><subject>Metalloproteinase</subject><subject>multidisciplinary</subject><subject>Muscle contraction</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myofibroblasts - cytology</subject><subject>Myofibroblasts - drug effects</subject><subject>Myofibroblasts - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Secretome</subject><subject>Signal Transduction</subject><subject>Stromal cells</subject><subject>Tissue inhibitor of metalloproteinase 2</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Transforming growth factor-b1</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNp9UstuFDEQHCEQiUJ-gAOyxIVDDH7OzlyQUMQGpEhcwtmyPe0dRzP2YnuC8lnwIXwTXjYsCwd8sFvuqnJ3u5rmOSWvKeHdmyyo7DtMaIe5WIkV5o-aU0aExIwz9vgoPmnOc74ldUnWC9o_bU44EZSvOD9tvq29SdFMOhe0SfFrGZHTtsSE2QUyS0EhFlRGQHrw25gBFZ_zAniA5O9gQLmkOOsJWZimjDLYBCXOcIF8GL3xJaObqzX-8Z1iH4bFVsbgnYMEoXhdfAwoOjQusw7I6jR4bZE7VJSrSolovo9Hd8-aJ05PGc4fzrPm8_r9zeUHfP3p6uPlu2ts6zgK7louBOdOy7oT66SURJAe2GA6xw0IrZ0wQLjuRAe6dz0diBCGSWNa7gw_a97udbeLmWGwteKkJ7VNftbpXkXt1d-Z4Ee1iXeqZayVlFaBVw8CKX5ZIBc1-7ybkw4Ql6wYrZ_DScdJhb78B3oblxRqezsUbSXpVztBtkfZFHNO4A7FUKJ2plB7U6hqCvXLFIpX0ovjNg6U3xaoAL4H5JoKG0h_3v6P7E9Mqcd3</recordid><startdate>20181109</startdate><enddate>20181109</enddate><creator>Liguori, Tácia Tavares Aquinas</creator><creator>Liguori, Gabriel Romero</creator><creator>Moreira, Luiz Felipe Pinho</creator><creator>Harmsen, Martin Conrad</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0179-4976</orcidid><orcidid>https://orcid.org/0000-0002-7128-2741</orcidid></search><sort><creationdate>20181109</creationdate><title>Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts</title><author>Liguori, Tácia Tavares Aquinas ; Liguori, Gabriel Romero ; Moreira, Luiz Felipe Pinho ; Harmsen, Martin Conrad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-8634433fa54330cf5550409e2db8f3be4aaf4be03a848ea9f91d044b25bb63fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13/100</topic><topic>14</topic><topic>14/1</topic><topic>14/63</topic><topic>38</topic><topic>38/77</topic><topic>38/90</topic><topic>631/532/2118/2074</topic><topic>692/4019/592/2725</topic><topic>82/80</topic><topic>Adipose tissue</topic><topic>Cell Differentiation - drug effects</topic><topic>Cells, Cultured</topic><topic>Collagen (type I)</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - metabolism</topic><topic>Fibers</topic><topic>Fibroblast growth factor 2</topic><topic>Fibroblast Growth Factor 2 - pharmacology</topic><topic>Fibroblasts</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Heart</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Mesenchymal Stem Cells - cytology</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Mesenchyme</topic><topic>Metalloproteinase</topic><topic>multidisciplinary</topic><topic>Muscle contraction</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myofibroblasts - cytology</topic><topic>Myofibroblasts - drug effects</topic><topic>Myofibroblasts - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Secretome</topic><topic>Signal Transduction</topic><topic>Stromal cells</topic><topic>Tissue inhibitor of metalloproteinase 2</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Transforming growth factor-b1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liguori, Tácia Tavares Aquinas</creatorcontrib><creatorcontrib>Liguori, Gabriel Romero</creatorcontrib><creatorcontrib>Moreira, Luiz Felipe Pinho</creatorcontrib><creatorcontrib>Harmsen, Martin Conrad</creatorcontrib><collection>Springer Nature OA Free Journals</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 One Sustainability</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>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>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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liguori, Tácia Tavares Aquinas</au><au>Liguori, Gabriel Romero</au><au>Moreira, Luiz Felipe Pinho</au><au>Harmsen, Martin Conrad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-11-09</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>16633</spage><epage>10</epage><pages>16633-10</pages><artnum>16633</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Transforming growth factor-β1 (TGF-β1) is a potent inducer of fibroblast to myofibroblast differentiation and contributes to the pro-fibrotic microenvironment during cardiac remodeling. Fibroblast growth factor-2 (FGF-2) is a growth factor secreted by adipose tissue-derived stromal cells (ASC) which can antagonize TGF-β1 signaling. We hypothesized that TGF-β1-induced cardiac fibroblast to myofibroblast differentiation is abrogated by FGF-2 and ASC conditioned medium (ASC-CMed). Our experiments demonstrated that TGF-β1 treatment-induced cardiac fibroblast differentiation into myofibroblasts, as evidenced by the formation of contractile stress fibers rich in αSMA. FGF-2 blocked the differentiation, as evidenced by the reduction in gene (
TAGLN
, p < 0.0001;
ACTA2
, p = 0.0056) and protein (αSMA, p = 0.0338) expression of mesenchymal markers and extracellular matrix components gene expression (
COL1A1
, p < 0.0001;
COL3A1
, p = 0.0029). ASC-CMed did not block myofibroblast differentiation. The treatment with FGF-2 increased matrix metalloproteinases gene expression (
MMP1
, p < 0.0001;
MMP14
, p = 0.0027) and decreased the expression of tissue inhibitor of metalloproteinase gene
TIMP2
(p = 0.0023). ASC-CMed did not influence these genes. The proliferation of TGF-β1-induced human cardiac fibroblasts was restored by both FGF-2 (p = 0.0002) and ASC-CMed (p = 0.0121). The present study supports the anti-fibrotic effects of FGF-2 through the blockage of cardiac fibroblast differentiation into myofibroblasts. ASC-CMed, however, did not replicate the anti-fibrotic effects of FGF-2
in vitro
.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30413733</pmid><doi>10.1038/s41598-018-34747-3</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-0179-4976</orcidid><orcidid>https://orcid.org/0000-0002-7128-2741</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 13/100 14 14/1 14/63 38 38/77 38/90 631/532/2118/2074 692/4019/592/2725 82/80 Adipose tissue Cell Differentiation - drug effects Cells, Cultured Collagen (type I) Culture Media, Conditioned - pharmacology Extracellular matrix Extracellular Matrix - metabolism Fibers Fibroblast growth factor 2 Fibroblast Growth Factor 2 - pharmacology Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism Gene expression Growth factors Heart Humanities and Social Sciences Humans Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - metabolism Mesenchyme Metalloproteinase multidisciplinary Muscle contraction Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myofibroblasts - cytology Myofibroblasts - drug effects Myofibroblasts - metabolism Science Science (multidisciplinary) Secretome Signal Transduction Stromal cells Tissue inhibitor of metalloproteinase 2 Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 |
| title | Fibroblast growth factor-2, but not the adipose tissue-derived stromal cells secretome, inhibits TGF-β1-induced differentiation of human cardiac fibroblasts into myofibroblasts |
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