CTGF increases vascular endothelial growth factor-dependent angiogenesis in human synovial fibroblasts by increasing miR-210 expression
Connective tissue growth factor (CTGF, a.k.a. CCN2) is inflammatory mediator and abundantly expressed in osteoarthritis (OA). Angiogenesis is essential for OA progression. Here, we investigated the role of CTGF in vascular endothelial growth factor (VEGF) production and angiogenesis in OA synovial f...
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| description | Connective tissue growth factor (CTGF, a.k.a. CCN2) is inflammatory mediator and abundantly expressed in osteoarthritis (OA). Angiogenesis is essential for OA progression. Here, we investigated the role of CTGF in vascular endothelial growth factor (VEGF) production and angiogenesis in OA synovial fibroblasts (OASFs). We showed that expression of CTGF and VEGF in synovial fluid were higher in OA patients than in controls. Directly applying CTGF to OASFs increased VEGF production then promoted endothelial progenitor cells tube formation and migration. CTGF induced VEGF by raising miR-210 expression via PI3K, AKT, ERK, and nuclear factor-
κ
B (NF-
κ
B)/ELK1 pathways. CTGF-mediating miR-210 upregulation repressed glycerol-3-phosphate dehydrogenase 1-like (GPD1L) expression and PHD activity and subsequently promoted hypoxia-inducible factor (HIF)-1
α
-dependent VEGF expression. Knockdown of CTGF decreased VEGF expression and abolished OASF-conditional medium-mediated angiogenesis
in vitro
as well as angiogenesis in chick chorioallantoic membrane and Matrigel-plug nude mice model
in vivo
. Taken together, our results suggest CTGF activates PI3K, AKT, ERK, and NF-
κ
B/ELK1 pathway, leading to the upregulation of miR-210, contributing to inhibit GPD1L expression and prolyl hydroxylases 2 activity, promoting HIF-1
α
-dependent VEGF expression and angiogenesis in human synovial fibroblasts. |
| doi_str_mv | 10.1038/cddis.2014.453 |
| format | Article |
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κ
B (NF-
κ
B)/ELK1 pathways. CTGF-mediating miR-210 upregulation repressed glycerol-3-phosphate dehydrogenase 1-like (GPD1L) expression and PHD activity and subsequently promoted hypoxia-inducible factor (HIF)-1
α
-dependent VEGF expression. Knockdown of CTGF decreased VEGF expression and abolished OASF-conditional medium-mediated angiogenesis
in vitro
as well as angiogenesis in chick chorioallantoic membrane and Matrigel-plug nude mice model
in vivo
. Taken together, our results suggest CTGF activates PI3K, AKT, ERK, and NF-
κ
B/ELK1 pathway, leading to the upregulation of miR-210, contributing to inhibit GPD1L expression and prolyl hydroxylases 2 activity, promoting HIF-1
α
-dependent VEGF expression and angiogenesis in human synovial fibroblasts.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2014.453</identifier><identifier>PMID: 25341039</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/44 ; 13/51 ; 13/89 ; 14/63 ; 38/15 ; 45/90 ; 631/337/384/331 ; 631/443/1338/16 ; 692/420 ; 692/699/1670/407 ; 82/29 ; 82/80 ; 96/1 ; 96/106 ; 96/109 ; 96/44 ; 96/95 ; Antibodies ; Biochemistry ; Biomedical and Life Sciences ; Case-Control Studies ; Cell Biology ; Cell Culture ; Connective Tissue Growth Factor - metabolism ; ets-Domain Protein Elk-1 - metabolism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Gene Knockdown Techniques ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism ; Immunology ; Life Sciences ; MicroRNAs - metabolism ; Models, Biological ; Neovascularization, Physiologic ; NF-kappa B - metabolism ; Original ; original-article ; Osteoarthritis - pathology ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Synovial Membrane - pathology ; Up-Regulation ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Cell death & disease, 2014-10, Vol.5 (10), p.e1485-e1485</ispartof><rights>The Author(s) 2014</rights><rights>Copyright Nature Publishing Group Oct 2014</rights><rights>Copyright © 2014 Macmillan Publishers Limited 2014 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-ae4d2dea93ac2025a9bd6f1661e4b9c897928ee475f9c46f43715275582ed9783</citedby><cites>FETCH-LOGICAL-c557t-ae4d2dea93ac2025a9bd6f1661e4b9c897928ee475f9c46f43715275582ed9783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4649533/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4649533/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,41101,42170,51557,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25341039$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, S-C</creatorcontrib><creatorcontrib>Chuang, S-M</creatorcontrib><creatorcontrib>Hsu, C-J</creatorcontrib><creatorcontrib>Tsai, C-H</creatorcontrib><creatorcontrib>Wang, S-W</creatorcontrib><creatorcontrib>Tang, C-H</creatorcontrib><title>CTGF increases vascular endothelial growth factor-dependent angiogenesis in human synovial fibroblasts by increasing miR-210 expression</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Connective tissue growth factor (CTGF, a.k.a. CCN2) is inflammatory mediator and abundantly expressed in osteoarthritis (OA). Angiogenesis is essential for OA progression. Here, we investigated the role of CTGF in vascular endothelial growth factor (VEGF) production and angiogenesis in OA synovial fibroblasts (OASFs). We showed that expression of CTGF and VEGF in synovial fluid were higher in OA patients than in controls. Directly applying CTGF to OASFs increased VEGF production then promoted endothelial progenitor cells tube formation and migration. CTGF induced VEGF by raising miR-210 expression via PI3K, AKT, ERK, and nuclear factor-
κ
B (NF-
κ
B)/ELK1 pathways. CTGF-mediating miR-210 upregulation repressed glycerol-3-phosphate dehydrogenase 1-like (GPD1L) expression and PHD activity and subsequently promoted hypoxia-inducible factor (HIF)-1
α
-dependent VEGF expression. Knockdown of CTGF decreased VEGF expression and abolished OASF-conditional medium-mediated angiogenesis
in vitro
as well as angiogenesis in chick chorioallantoic membrane and Matrigel-plug nude mice model
in vivo
. Taken together, our results suggest CTGF activates PI3K, AKT, ERK, and NF-
κ
B/ELK1 pathway, leading to the upregulation of miR-210, contributing to inhibit GPD1L expression and prolyl hydroxylases 2 activity, promoting HIF-1
α
-dependent VEGF expression and angiogenesis in human synovial fibroblasts.</description><subject>13/44</subject><subject>13/51</subject><subject>13/89</subject><subject>14/63</subject><subject>38/15</subject><subject>45/90</subject><subject>631/337/384/331</subject><subject>631/443/1338/16</subject><subject>692/420</subject><subject>692/699/1670/407</subject><subject>82/29</subject><subject>82/80</subject><subject>96/1</subject><subject>96/106</subject><subject>96/109</subject><subject>96/44</subject><subject>96/95</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Case-Control Studies</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>ets-Domain Protein Elk-1 - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - pathology</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>MicroRNAs - metabolism</subject><subject>Models, Biological</subject><subject>Neovascularization, Physiologic</subject><subject>NF-kappa B - metabolism</subject><subject>Original</subject><subject>original-article</subject><subject>Osteoarthritis - pathology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Synovial Membrane - pathology</subject><subject>Up-Regulation</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNqFkk9r3DAQxU1paUKaa49F0Esv3lh_bV0KZWmSQqBQ0rOQ5bFXwSttNfam-wn6tavNJmFbCtVFgvebNxrpFcVbWi1oxZsL13UeF6yiYiEkf1GcskrQUjSNfnl0PinOEe-qvDivmFSvixMmucgO-rT4tby9uiQ-uAQWAcnWoptHmwiELk4rGL0dyZDi_bQivXVTTGUHmyxCmIgNg48DBECP2YOs5rUNBHchbvdlvW9TbEeLE5J299TEh4Gs_beS0YrAz00CRB_Dm-JVb0eE88f9rPh--fl2eV3efL36svx0Uzop66m0IDrWgdXcOpaHsbrtVE-VoiBa7Rpda9YAiFr22gnVC15TyWopGwadrht-Vnw8-G7mdg2dy2MkO5pN8mubdiZab_5Ugl-ZIW6NUEJLzrPBh0eDFH_MgJNZe3QwjjZAnNHQWldaMS2r_6OKNlRSpVVG3_-F3sU5hfwS2bBRjDOmWaYWB8qliJigf743rcw-EeYhEWafCJMTkQveHU_7jD_9fwYuDgBmKQyQjvr-2_I3LkPEKA</recordid><startdate>20141023</startdate><enddate>20141023</enddate><creator>Liu, S-C</creator><creator>Chuang, S-M</creator><creator>Hsu, C-J</creator><creator>Tsai, C-H</creator><creator>Wang, S-W</creator><creator>Tang, C-H</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</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>88I</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</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>7TO</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20141023</creationdate><title>CTGF increases vascular endothelial growth factor-dependent angiogenesis in human synovial fibroblasts by increasing miR-210 expression</title><author>Liu, S-C ; Chuang, S-M ; Hsu, C-J ; Tsai, C-H ; Wang, S-W ; Tang, C-H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-ae4d2dea93ac2025a9bd6f1661e4b9c897928ee475f9c46f43715275582ed9783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>13/44</topic><topic>13/51</topic><topic>13/89</topic><topic>14/63</topic><topic>38/15</topic><topic>45/90</topic><topic>631/337/384/331</topic><topic>631/443/1338/16</topic><topic>692/420</topic><topic>692/699/1670/407</topic><topic>82/29</topic><topic>82/80</topic><topic>96/1</topic><topic>96/106</topic><topic>96/109</topic><topic>96/44</topic><topic>96/95</topic><topic>Antibodies</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Case-Control Studies</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>ets-Domain Protein Elk-1 - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - pathology</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism</topic><topic>Immunology</topic><topic>Life Sciences</topic><topic>MicroRNAs - metabolism</topic><topic>Models, Biological</topic><topic>Neovascularization, Physiologic</topic><topic>NF-kappa B - metabolism</topic><topic>Original</topic><topic>original-article</topic><topic>Osteoarthritis - pathology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Synovial Membrane - pathology</topic><topic>Up-Regulation</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, S-C</creatorcontrib><creatorcontrib>Chuang, S-M</creatorcontrib><creatorcontrib>Hsu, C-J</creatorcontrib><creatorcontrib>Tsai, C-H</creatorcontrib><creatorcontrib>Wang, S-W</creatorcontrib><creatorcontrib>Tang, C-H</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>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 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>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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, S-C</au><au>Chuang, S-M</au><au>Hsu, C-J</au><au>Tsai, C-H</au><au>Wang, S-W</au><au>Tang, C-H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CTGF increases vascular endothelial growth factor-dependent angiogenesis in human synovial fibroblasts by increasing miR-210 expression</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2014-10-23</date><risdate>2014</risdate><volume>5</volume><issue>10</issue><spage>e1485</spage><epage>e1485</epage><pages>e1485-e1485</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Connective tissue growth factor (CTGF, a.k.a. CCN2) is inflammatory mediator and abundantly expressed in osteoarthritis (OA). Angiogenesis is essential for OA progression. Here, we investigated the role of CTGF in vascular endothelial growth factor (VEGF) production and angiogenesis in OA synovial fibroblasts (OASFs). We showed that expression of CTGF and VEGF in synovial fluid were higher in OA patients than in controls. Directly applying CTGF to OASFs increased VEGF production then promoted endothelial progenitor cells tube formation and migration. CTGF induced VEGF by raising miR-210 expression via PI3K, AKT, ERK, and nuclear factor-
κ
B (NF-
κ
B)/ELK1 pathways. CTGF-mediating miR-210 upregulation repressed glycerol-3-phosphate dehydrogenase 1-like (GPD1L) expression and PHD activity and subsequently promoted hypoxia-inducible factor (HIF)-1
α
-dependent VEGF expression. Knockdown of CTGF decreased VEGF expression and abolished OASF-conditional medium-mediated angiogenesis
in vitro
as well as angiogenesis in chick chorioallantoic membrane and Matrigel-plug nude mice model
in vivo
. Taken together, our results suggest CTGF activates PI3K, AKT, ERK, and NF-
κ
B/ELK1 pathway, leading to the upregulation of miR-210, contributing to inhibit GPD1L expression and prolyl hydroxylases 2 activity, promoting HIF-1
α
-dependent VEGF expression and angiogenesis in human synovial fibroblasts.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25341039</pmid><doi>10.1038/cddis.2014.453</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; Nature Free; PubMed Central |
| subjects | 13/44 13/51 13/89 14/63 38/15 45/90 631/337/384/331 631/443/1338/16 692/420 692/699/1670/407 82/29 82/80 96/1 96/106 96/109 96/44 96/95 Antibodies Biochemistry Biomedical and Life Sciences Case-Control Studies Cell Biology Cell Culture Connective Tissue Growth Factor - metabolism ets-Domain Protein Elk-1 - metabolism Extracellular Signal-Regulated MAP Kinases - metabolism Fibroblasts - metabolism Fibroblasts - pathology Gene Knockdown Techniques Humans Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-Inducible Factor-Proline Dioxygenases - metabolism Immunology Life Sciences MicroRNAs - metabolism Models, Biological Neovascularization, Physiologic NF-kappa B - metabolism Original original-article Osteoarthritis - pathology Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Synovial Membrane - pathology Up-Regulation Vascular Endothelial Growth Factor A - metabolism |
| title | CTGF increases vascular endothelial growth factor-dependent angiogenesis in human synovial fibroblasts by increasing miR-210 expression |
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