Functional cooperation between vitamin D receptor and Runx2 in vitamin D-induced vascular calcification
The transdifferentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells has been implicated in the context of vascular calcification. We investigated the roles of vitamin D receptor (Vdr) and runt-related transcription factor 2 (Runx2) in the osteoblastic differentiation of VSMCs...
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creator | Han, Min-Su Che, Xiangguo Cho, Gyoung-ho Park, Hye-Ri Lim, Kyung-Eun Park, Na-Rae Jin, Jung-Sook Jung, Youn-Kwan Jeong, Jae-Hwan Lee, In-Kyu Kato, Shigeaki Choi, Je-Yong |
description | The transdifferentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells has been implicated in the context of vascular calcification. We investigated the roles of vitamin D receptor (Vdr) and runt-related transcription factor 2 (Runx2) in the osteoblastic differentiation of VSMCs in response to vitamin D3 using in vitro VSMCs cultures and in vivo in Vdr knockout (Vdr(-/-)) and Runx2 carboxy-terminus truncated heterozygous (Runx2(+/ΔC)) mice. Treatment of VSMCs with active vitamin D3 promoted matrix mineral deposition, and increased the expressions of Vdr, Runx2, and of osteoblastic genes but decreased the expression of smooth muscle myosin heavy chain in primary VSMCs cultures. Immunoprecipitation experiments suggested an interaction between Vdr and Runx2. Furthermore, silencing Vdr or Runx2 attenuated the procalcific effects of vitamin D3. Functional cooperation between Vdr and Runx2 in vascular calcification was also confirmed in in vivo mouse models. Vascular calcification induced by high-dose vitamin D3 was completely inhibited in Vdr(-/-) or Runx2(+/ΔC) mice, despite elevated levels of serum calcium or alkaline phosphatase. Collectively, these findings suggest that functional cooperation between Vdr and Runx2 is necessary for vascular calcification in response to vitamin D3. |
doi_str_mv | 10.1371/journal.pone.0083584 |
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We investigated the roles of vitamin D receptor (Vdr) and runt-related transcription factor 2 (Runx2) in the osteoblastic differentiation of VSMCs in response to vitamin D3 using in vitro VSMCs cultures and in vivo in Vdr knockout (Vdr(-/-)) and Runx2 carboxy-terminus truncated heterozygous (Runx2(+/ΔC)) mice. Treatment of VSMCs with active vitamin D3 promoted matrix mineral deposition, and increased the expressions of Vdr, Runx2, and of osteoblastic genes but decreased the expression of smooth muscle myosin heavy chain in primary VSMCs cultures. Immunoprecipitation experiments suggested an interaction between Vdr and Runx2. Furthermore, silencing Vdr or Runx2 attenuated the procalcific effects of vitamin D3. Functional cooperation between Vdr and Runx2 in vascular calcification was also confirmed in in vivo mouse models. Vascular calcification induced by high-dose vitamin D3 was completely inhibited in Vdr(-/-) or Runx2(+/ΔC) mice, despite elevated levels of serum calcium or alkaline phosphatase. Collectively, these findings suggest that functional cooperation between Vdr and Runx2 is necessary for vascular calcification in response to vitamin D3.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0083584</identifier><identifier>PMID: 24349534</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alkaline phosphatase ; Animal models ; Animals ; Biochemistry ; Biocompatibility ; Biology ; Biomedical materials ; Bone Density Conservation Agents - adverse effects ; Bone Density Conservation Agents - pharmacology ; Calcification ; Calcification (ectopic) ; Calcification (Physiology) ; Calcium ; Calcium (blood) ; Cbfa-1 protein ; Cells, Cultured ; Cholecalciferol - adverse effects ; Cholecalciferol - pharmacology ; Cooperation ; Cooperativity ; Core Binding Factor Alpha 1 Subunit - genetics ; Core Binding Factor Alpha 1 Subunit - metabolism ; Endocrinology ; Gene expression ; Genomes ; Growth factors ; Homeostasis ; Immunoprecipitation ; Kidneys ; Ligands ; Medicine ; Mice ; Mice, Knockout ; Muscle proteins ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Muscles ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; Myosin ; Osteoblastogenesis ; Osteoblasts ; Phosphatases ; Polyclonal antibodies ; Proteins ; Rats ; Receptors, Calcitriol - genetics ; Receptors, Calcitriol - metabolism ; Rodents ; Smooth muscle ; Transcription factors ; Vascular Calcification - chemically induced ; Vascular Calcification - genetics ; Vascular Calcification - metabolism ; Vascular Calcification - pathology ; Vitamin D ; Vitamin D receptors ; Vitamin D3 ; Vitamin deficiency</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e83584</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Han 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>2013 Han et al 2013 Han et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-bc18313eca3fa1091664924d050ce388777e799794447946d7b4ac2f57573f503</citedby><cites>FETCH-LOGICAL-c758t-bc18313eca3fa1091664924d050ce388777e799794447946d7b4ac2f57573f503</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/PMC3861528/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3861528/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24349534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Min-Su</creatorcontrib><creatorcontrib>Che, Xiangguo</creatorcontrib><creatorcontrib>Cho, Gyoung-ho</creatorcontrib><creatorcontrib>Park, Hye-Ri</creatorcontrib><creatorcontrib>Lim, Kyung-Eun</creatorcontrib><creatorcontrib>Park, Na-Rae</creatorcontrib><creatorcontrib>Jin, Jung-Sook</creatorcontrib><creatorcontrib>Jung, Youn-Kwan</creatorcontrib><creatorcontrib>Jeong, Jae-Hwan</creatorcontrib><creatorcontrib>Lee, In-Kyu</creatorcontrib><creatorcontrib>Kato, Shigeaki</creatorcontrib><creatorcontrib>Choi, Je-Yong</creatorcontrib><title>Functional cooperation between vitamin D receptor and Runx2 in vitamin D-induced vascular calcification</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The transdifferentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells has been implicated in the context of vascular calcification. We investigated the roles of vitamin D receptor (Vdr) and runt-related transcription factor 2 (Runx2) in the osteoblastic differentiation of VSMCs in response to vitamin D3 using in vitro VSMCs cultures and in vivo in Vdr knockout (Vdr(-/-)) and Runx2 carboxy-terminus truncated heterozygous (Runx2(+/ΔC)) mice. Treatment of VSMCs with active vitamin D3 promoted matrix mineral deposition, and increased the expressions of Vdr, Runx2, and of osteoblastic genes but decreased the expression of smooth muscle myosin heavy chain in primary VSMCs cultures. Immunoprecipitation experiments suggested an interaction between Vdr and Runx2. Furthermore, silencing Vdr or Runx2 attenuated the procalcific effects of vitamin D3. Functional cooperation between Vdr and Runx2 in vascular calcification was also confirmed in in vivo mouse models. Vascular calcification induced by high-dose vitamin D3 was completely inhibited in Vdr(-/-) or Runx2(+/ΔC) mice, despite elevated levels of serum calcium or alkaline phosphatase. Collectively, these findings suggest that functional cooperation between Vdr and Runx2 is necessary for vascular calcification in response to vitamin D3.</description><subject>Alkaline phosphatase</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>Biomedical materials</subject><subject>Bone Density Conservation Agents - adverse effects</subject><subject>Bone Density Conservation Agents - pharmacology</subject><subject>Calcification</subject><subject>Calcification (ectopic)</subject><subject>Calcification (Physiology)</subject><subject>Calcium</subject><subject>Calcium (blood)</subject><subject>Cbfa-1 protein</subject><subject>Cells, Cultured</subject><subject>Cholecalciferol - adverse effects</subject><subject>Cholecalciferol - pharmacology</subject><subject>Cooperation</subject><subject>Cooperativity</subject><subject>Core Binding Factor Alpha 1 Subunit - genetics</subject><subject>Core Binding Factor Alpha 1 Subunit - metabolism</subject><subject>Endocrinology</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Growth factors</subject><subject>Homeostasis</subject><subject>Immunoprecipitation</subject><subject>Kidneys</subject><subject>Ligands</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle proteins</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Muscles</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>Myosin</subject><subject>Osteoblastogenesis</subject><subject>Osteoblasts</subject><subject>Phosphatases</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptors, Calcitriol - genetics</subject><subject>Receptors, Calcitriol - metabolism</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Transcription factors</subject><subject>Vascular Calcification - chemically induced</subject><subject>Vascular Calcification - genetics</subject><subject>Vascular Calcification - metabolism</subject><subject>Vascular Calcification - pathology</subject><subject>Vitamin D</subject><subject>Vitamin D receptors</subject><subject>Vitamin D3</subject><subject>Vitamin deficiency</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl-L1DAUxYso7rr6DUQLguDDjEmTNumLsKyuDiwsrH9ew216O5Ohk4xJOq7f3sxOd5mCggSa9OZ3Ty-nJ8teUjKnTND3azd4C_186yzOCZGslPxRdkprVsyqgrDHR-eT7FkIa0JKJqvqaXZScMbrkvHTbHk5WB2NS0q5dm6LHvZveYPxF6LNdybCxtj8Y-5R4zY6n4Nt85vB3ha5ObqfGdsOGtt8B0EPPfhcQ69NZ_Sd4PPsSQd9wBfjfpZ9v_z07eLL7Or68-Li_GqmRSnjrNFUMspQA-uAkppWFa8L3pKSaGRSCiFQ1LWoOefpUbWi4aCLrhSlYF1J2Fn2-qC77V1Qo0dBUS64LIWQRSIWB6J1sFZbbzbgfysHRt0VnF8q8NHoHlVNsEEKlSSs4ZwQ6BihbUEKJjuOVZ20PoxfG5oNthpt9NBPRKc31qzU0u1U-g-0LGQSeDMKePdzwBD_MfJILSFNZWznkpjemKDVORfJMCL4fpj5X6i0WtwYnVLSmVSfNLybNCQm4m1cwhCCWny9-X_2-seUfXvErhD6uAquH_Y5CFOQH0DtXQgeuwfnKFH7kN-7ofYhV2PIU9urY9cfmu5Tzf4AWu72cg</recordid><startdate>20131212</startdate><enddate>20131212</enddate><creator>Han, Min-Su</creator><creator>Che, Xiangguo</creator><creator>Cho, Gyoung-ho</creator><creator>Park, Hye-Ri</creator><creator>Lim, Kyung-Eun</creator><creator>Park, Na-Rae</creator><creator>Jin, Jung-Sook</creator><creator>Jung, Youn-Kwan</creator><creator>Jeong, Jae-Hwan</creator><creator>Lee, In-Kyu</creator><creator>Kato, Shigeaki</creator><creator>Choi, Je-Yong</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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131212</creationdate><title>Functional cooperation between vitamin D receptor and Runx2 in vitamin D-induced vascular calcification</title><author>Han, Min-Su ; Che, Xiangguo ; Cho, Gyoung-ho ; Park, Hye-Ri ; Lim, Kyung-Eun ; Park, Na-Rae ; Jin, Jung-Sook ; Jung, Youn-Kwan ; Jeong, Jae-Hwan ; Lee, In-Kyu ; Kato, Shigeaki ; Choi, Je-Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-bc18313eca3fa1091664924d050ce388777e799794447946d7b4ac2f57573f503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alkaline phosphatase</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biocompatibility</topic><topic>Biology</topic><topic>Biomedical materials</topic><topic>Bone Density Conservation Agents - adverse effects</topic><topic>Bone Density Conservation Agents - pharmacology</topic><topic>Calcification</topic><topic>Calcification (ectopic)</topic><topic>Calcification (Physiology)</topic><topic>Calcium</topic><topic>Calcium (blood)</topic><topic>Cbfa-1 protein</topic><topic>Cells, Cultured</topic><topic>Cholecalciferol - adverse effects</topic><topic>Cholecalciferol - pharmacology</topic><topic>Cooperation</topic><topic>Cooperativity</topic><topic>Core Binding Factor Alpha 1 Subunit - genetics</topic><topic>Core Binding Factor Alpha 1 Subunit - metabolism</topic><topic>Endocrinology</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Growth factors</topic><topic>Homeostasis</topic><topic>Immunoprecipitation</topic><topic>Kidneys</topic><topic>Ligands</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Muscle proteins</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Muscles</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Myocytes, Smooth Muscle - pathology</topic><topic>Myosin</topic><topic>Osteoblastogenesis</topic><topic>Osteoblasts</topic><topic>Phosphatases</topic><topic>Polyclonal antibodies</topic><topic>Proteins</topic><topic>Rats</topic><topic>Receptors, Calcitriol - genetics</topic><topic>Receptors, Calcitriol - metabolism</topic><topic>Rodents</topic><topic>Smooth muscle</topic><topic>Transcription factors</topic><topic>Vascular Calcification - chemically induced</topic><topic>Vascular Calcification - genetics</topic><topic>Vascular Calcification - metabolism</topic><topic>Vascular Calcification - pathology</topic><topic>Vitamin D</topic><topic>Vitamin D receptors</topic><topic>Vitamin D3</topic><topic>Vitamin deficiency</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Min-Su</creatorcontrib><creatorcontrib>Che, Xiangguo</creatorcontrib><creatorcontrib>Cho, Gyoung-ho</creatorcontrib><creatorcontrib>Park, Hye-Ri</creatorcontrib><creatorcontrib>Lim, Kyung-Eun</creatorcontrib><creatorcontrib>Park, Na-Rae</creatorcontrib><creatorcontrib>Jin, Jung-Sook</creatorcontrib><creatorcontrib>Jung, Youn-Kwan</creatorcontrib><creatorcontrib>Jeong, Jae-Hwan</creatorcontrib><creatorcontrib>Lee, In-Kyu</creatorcontrib><creatorcontrib>Kato, Shigeaki</creatorcontrib><creatorcontrib>Choi, Je-Yong</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 One Sustainability</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 - 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We investigated the roles of vitamin D receptor (Vdr) and runt-related transcription factor 2 (Runx2) in the osteoblastic differentiation of VSMCs in response to vitamin D3 using in vitro VSMCs cultures and in vivo in Vdr knockout (Vdr(-/-)) and Runx2 carboxy-terminus truncated heterozygous (Runx2(+/ΔC)) mice. Treatment of VSMCs with active vitamin D3 promoted matrix mineral deposition, and increased the expressions of Vdr, Runx2, and of osteoblastic genes but decreased the expression of smooth muscle myosin heavy chain in primary VSMCs cultures. Immunoprecipitation experiments suggested an interaction between Vdr and Runx2. Furthermore, silencing Vdr or Runx2 attenuated the procalcific effects of vitamin D3. Functional cooperation between Vdr and Runx2 in vascular calcification was also confirmed in in vivo mouse models. Vascular calcification induced by high-dose vitamin D3 was completely inhibited in Vdr(-/-) or Runx2(+/ΔC) mice, despite elevated levels of serum calcium or alkaline phosphatase. Collectively, these findings suggest that functional cooperation between Vdr and Runx2 is necessary for vascular calcification in response to vitamin D3.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24349534</pmid><doi>10.1371/journal.pone.0083584</doi><tpages>e83584</tpages><oa>free_for_read</oa></addata></record> |
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recordid | cdi_plos_journals_1474857782 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | Alkaline phosphatase Animal models Animals Biochemistry Biocompatibility Biology Biomedical materials Bone Density Conservation Agents - adverse effects Bone Density Conservation Agents - pharmacology Calcification Calcification (ectopic) Calcification (Physiology) Calcium Calcium (blood) Cbfa-1 protein Cells, Cultured Cholecalciferol - adverse effects Cholecalciferol - pharmacology Cooperation Cooperativity Core Binding Factor Alpha 1 Subunit - genetics Core Binding Factor Alpha 1 Subunit - metabolism Endocrinology Gene expression Genomes Growth factors Homeostasis Immunoprecipitation Kidneys Ligands Medicine Mice Mice, Knockout Muscle proteins Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Muscles Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology Myosin Osteoblastogenesis Osteoblasts Phosphatases Polyclonal antibodies Proteins Rats Receptors, Calcitriol - genetics Receptors, Calcitriol - metabolism Rodents Smooth muscle Transcription factors Vascular Calcification - chemically induced Vascular Calcification - genetics Vascular Calcification - metabolism Vascular Calcification - pathology Vitamin D Vitamin D receptors Vitamin D3 Vitamin deficiency |
title | Functional cooperation between vitamin D receptor and Runx2 in vitamin D-induced vascular calcification |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T22%3A18%3A39IST&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=Functional%20cooperation%20between%20vitamin%20D%20receptor%20and%20Runx2%20in%20vitamin%20D-induced%20vascular%20calcification&rft.jtitle=PloS%20one&rft.au=Han,%20Min-Su&rft.date=2013-12-12&rft.volume=8&rft.issue=12&rft.spage=e83584&rft.pages=e83584-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0083584&rft_dat=%3Cgale_plos_%3EA478310749%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=1474857782&rft_id=info:pmid/24349534&rft_galeid=A478310749&rft_doaj_id=oai_doaj_org_article_90ebe1a6803b4400af301d20238f4e69&rfr_iscdi=true |