Ascorbic acid promotes a TGF β 1-induced myofibroblast phenotype switch
l-Ascorbic acid (AA), generally known as vitamin C, is a crucial cofactor for a variety of enzymes, including prolyl-3-hydroxylase (P3H), prolyl-4-hydroxylase (P4H), and lysyl hydroxylase (LH)-mediated collagen maturation. Here, we investigated whether AA has additional functions in the regulation o...
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| Veröffentlicht in: | Physiological reports 2017-09, Vol.5 (17), p.e13324 |
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| creator | Piersma, Bram Wouters, Olaf Y de Rond, Saskia Boersema, Miriam Gjaltema, Rutger A F Bank, Ruud A |
| description | l-Ascorbic acid (AA), generally known as vitamin C, is a crucial cofactor for a variety of enzymes, including prolyl-3-hydroxylase (P3H), prolyl-4-hydroxylase (P4H), and lysyl hydroxylase (LH)-mediated collagen maturation. Here, we investigated whether AA has additional functions in the regulation of the myofibroblast phenotype, besides its function in collagen biosynthesis. We found that AA positively influences TGF
1-induced expression of
,
, and
Moreover, we demonstrated that AA promotes
SMA stress fiber formation as well as the synthesis and deposition of collagens type I and IV Additionally, AA amplified the contractile phenotype of the myofibroblasts, as seen by increased contraction of a 3D collagen lattice. Moreover, AA increased the expression of several TGF
1-induced genes, including
and
Finally, we demonstrated that the mechanism of AA action seems independent of Smad2/3 signaling. |
| doi_str_mv | 10.14814/phy2.13324 |
| format | Article |
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1-induced expression of
,
, and
Moreover, we demonstrated that AA promotes
SMA stress fiber formation as well as the synthesis and deposition of collagens type I and IV Additionally, AA amplified the contractile phenotype of the myofibroblasts, as seen by increased contraction of a 3D collagen lattice. Moreover, AA increased the expression of several TGF
1-induced genes, including
and
Finally, we demonstrated that the mechanism of AA action seems independent of Smad2/3 signaling.</description><identifier>EISSN: 2051-817X</identifier><identifier>DOI: 10.14814/phy2.13324</identifier><identifier>PMID: 28904079</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Actins - genetics ; Actins - metabolism ; Ascorbic acid ; Ascorbic Acid - pharmacology ; Cells, Cultured ; Collagen ; Collagen (type I) ; Collagen Type I - genetics ; Collagen Type I - metabolism ; Collagen Type IV - genetics ; Collagen Type IV - metabolism ; Connective tissue growth factor ; Connective Tissue Growth Factor - genetics ; Connective Tissue Growth Factor - metabolism ; Contractility ; Contraction ; Discoidin Domain Receptor 1 - genetics ; Discoidin Domain Receptor 1 - metabolism ; Enzymes ; Genotype & phenotype ; Humans ; Hydroxylase ; Myofibroblasts - cytology ; Myofibroblasts - drug effects ; Myofibroblasts - metabolism ; Phenotype ; Physiology ; Procollagen-lysine 5-dioxygenase ; Smad Proteins - metabolism ; Smad2 protein ; Transforming Growth Factor beta - pharmacology ; Transforming growth factor-b1 ; Vitamin C ; Vitamins - pharmacology</subject><ispartof>Physiological reports, 2017-09, Vol.5 (17), p.e13324</ispartof><rights>2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.</rights><rights>2017. 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-c1299-b6bc21ad7a550900f243fee5472ea919e517156362bf68e0590e1ac42be1ca553</citedby><cites>FETCH-LOGICAL-c1299-b6bc21ad7a550900f243fee5472ea919e517156362bf68e0590e1ac42be1ca553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28904079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Piersma, Bram</creatorcontrib><creatorcontrib>Wouters, Olaf Y</creatorcontrib><creatorcontrib>de Rond, Saskia</creatorcontrib><creatorcontrib>Boersema, Miriam</creatorcontrib><creatorcontrib>Gjaltema, Rutger A F</creatorcontrib><creatorcontrib>Bank, Ruud A</creatorcontrib><title>Ascorbic acid promotes a TGF β 1-induced myofibroblast phenotype switch</title><title>Physiological reports</title><addtitle>Physiol Rep</addtitle><description>l-Ascorbic acid (AA), generally known as vitamin C, is a crucial cofactor for a variety of enzymes, including prolyl-3-hydroxylase (P3H), prolyl-4-hydroxylase (P4H), and lysyl hydroxylase (LH)-mediated collagen maturation. Here, we investigated whether AA has additional functions in the regulation of the myofibroblast phenotype, besides its function in collagen biosynthesis. We found that AA positively influences TGF
1-induced expression of
,
, and
Moreover, we demonstrated that AA promotes
SMA stress fiber formation as well as the synthesis and deposition of collagens type I and IV Additionally, AA amplified the contractile phenotype of the myofibroblasts, as seen by increased contraction of a 3D collagen lattice. Moreover, AA increased the expression of several TGF
1-induced genes, including
and
Finally, we demonstrated that the mechanism of AA action seems independent of Smad2/3 signaling.</description><subject>Actins - genetics</subject><subject>Actins - metabolism</subject><subject>Ascorbic acid</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type IV - genetics</subject><subject>Collagen Type IV - metabolism</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - genetics</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Contractility</subject><subject>Contraction</subject><subject>Discoidin Domain Receptor 1 - genetics</subject><subject>Discoidin Domain Receptor 1 - metabolism</subject><subject>Enzymes</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Hydroxylase</subject><subject>Myofibroblasts - cytology</subject><subject>Myofibroblasts - drug effects</subject><subject>Myofibroblasts - metabolism</subject><subject>Phenotype</subject><subject>Physiology</subject><subject>Procollagen-lysine 5-dioxygenase</subject><subject>Smad Proteins - metabolism</subject><subject>Smad2 protein</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming growth factor-b1</subject><subject>Vitamin C</subject><subject>Vitamins - pharmacology</subject><issn>2051-817X</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><recordid>eNo9kM1KAzEUhYMgttSu3EvApUy9N8n8ZFmKbYWCmwruhiSToVM6zZjMIPNaPojP5NhWV2fz3XMuHyF3CDMUGYqnZtezGXLOxBUZM4gxyjB9H5FpCHsAQOBcgrghI5YNCakck_U8GOd1ZagyVUEb72rX2kAV3a6W9PuLYlQdi87Ygta9KyvtnT6o0NJmZ4-u7RtLw2fVmt0tuS7VIdjpJSfkbfm8XayjzevqZTHfRAaZlJFOtGGoilTFMUiAkgleWhuLlFklUdoYU4wTnjBdJpmFWIJFZQTTFs1wwyfk4dw7vPrR2dDme9f54zCZo-RZBqmQ6UA9ninjXQjelnnjq1r5PkfIT7LyX1n5SdZA3186O13b4p_908R_AJ20ZgQ</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Piersma, Bram</creator><creator>Wouters, Olaf Y</creator><creator>de Rond, Saskia</creator><creator>Boersema, Miriam</creator><creator>Gjaltema, Rutger A F</creator><creator>Bank, Ruud A</creator><general>John Wiley & Sons, Inc</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>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope></search><sort><creationdate>201709</creationdate><title>Ascorbic acid promotes a TGF β 1-induced myofibroblast phenotype switch</title><author>Piersma, Bram ; Wouters, Olaf Y ; de Rond, Saskia ; Boersema, Miriam ; Gjaltema, Rutger A F ; Bank, Ruud A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1299-b6bc21ad7a550900f243fee5472ea919e517156362bf68e0590e1ac42be1ca553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Actins - genetics</topic><topic>Actins - metabolism</topic><topic>Ascorbic acid</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type IV - genetics</topic><topic>Collagen Type IV - metabolism</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - genetics</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Contractility</topic><topic>Contraction</topic><topic>Discoidin Domain Receptor 1 - genetics</topic><topic>Discoidin Domain Receptor 1 - metabolism</topic><topic>Enzymes</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Hydroxylase</topic><topic>Myofibroblasts - cytology</topic><topic>Myofibroblasts - drug effects</topic><topic>Myofibroblasts - metabolism</topic><topic>Phenotype</topic><topic>Physiology</topic><topic>Procollagen-lysine 5-dioxygenase</topic><topic>Smad Proteins - metabolism</topic><topic>Smad2 protein</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Transforming growth factor-b1</topic><topic>Vitamin C</topic><topic>Vitamins - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Piersma, Bram</creatorcontrib><creatorcontrib>Wouters, Olaf Y</creatorcontrib><creatorcontrib>de Rond, Saskia</creatorcontrib><creatorcontrib>Boersema, Miriam</creatorcontrib><creatorcontrib>Gjaltema, Rutger A F</creatorcontrib><creatorcontrib>Bank, Ruud A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>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>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><jtitle>Physiological reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Piersma, Bram</au><au>Wouters, Olaf Y</au><au>de Rond, Saskia</au><au>Boersema, Miriam</au><au>Gjaltema, Rutger A F</au><au>Bank, Ruud A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ascorbic acid promotes a TGF β 1-induced myofibroblast phenotype switch</atitle><jtitle>Physiological reports</jtitle><addtitle>Physiol Rep</addtitle><date>2017-09</date><risdate>2017</risdate><volume>5</volume><issue>17</issue><spage>e13324</spage><pages>e13324-</pages><eissn>2051-817X</eissn><abstract>l-Ascorbic acid (AA), generally known as vitamin C, is a crucial cofactor for a variety of enzymes, including prolyl-3-hydroxylase (P3H), prolyl-4-hydroxylase (P4H), and lysyl hydroxylase (LH)-mediated collagen maturation. Here, we investigated whether AA has additional functions in the regulation of the myofibroblast phenotype, besides its function in collagen biosynthesis. We found that AA positively influences TGF
1-induced expression of
,
, and
Moreover, we demonstrated that AA promotes
SMA stress fiber formation as well as the synthesis and deposition of collagens type I and IV Additionally, AA amplified the contractile phenotype of the myofibroblasts, as seen by increased contraction of a 3D collagen lattice. Moreover, AA increased the expression of several TGF
1-induced genes, including
and
Finally, we demonstrated that the mechanism of AA action seems independent of Smad2/3 signaling.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>28904079</pmid><doi>10.14814/phy2.13324</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | Physiological reports, 2017-09, Vol.5 (17), p.e13324 |
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| subjects | Actins - genetics Actins - metabolism Ascorbic acid Ascorbic Acid - pharmacology Cells, Cultured Collagen Collagen (type I) Collagen Type I - genetics Collagen Type I - metabolism Collagen Type IV - genetics Collagen Type IV - metabolism Connective tissue growth factor Connective Tissue Growth Factor - genetics Connective Tissue Growth Factor - metabolism Contractility Contraction Discoidin Domain Receptor 1 - genetics Discoidin Domain Receptor 1 - metabolism Enzymes Genotype & phenotype Humans Hydroxylase Myofibroblasts - cytology Myofibroblasts - drug effects Myofibroblasts - metabolism Phenotype Physiology Procollagen-lysine 5-dioxygenase Smad Proteins - metabolism Smad2 protein Transforming Growth Factor beta - pharmacology Transforming growth factor-b1 Vitamin C Vitamins - pharmacology |
| title | Ascorbic acid promotes a TGF β 1-induced myofibroblast phenotype switch |
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