Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway
Plasticity of vascular smooth muscle cells (VSMCs) plays a central role in the onset and progression of proliferative vascular diseases. In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high...
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| description | Plasticity of vascular smooth muscle cells (VSMCs) plays a central role in the onset and progression of proliferative vascular diseases. In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high expression of contractile marker proteins. After injury to the vessel, VSMC shifts from a contractile phenotype to a pathological synthetic phenotype, associated with increased proliferation, migration and matrix secretion. It has been demonstrated that PDGF-BB is a critical mediator of VSMCs phenotypic switch. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methyl-glutaryl l coenzyme A (HMG-CoA) reductase, exhibits various protective effects against VSMCs. In this study, we investigated the effects of atorvastatin calcium on phenotype modulation of PDGF-BB-induced VSMCs and the related intracellular signal transduction pathways. Treatment of VSMCs with atorvastatin calcium showed dose-dependent inhibition of PDGF-BB-induced proliferation. Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs. Although Akt phosphorylation was strongly elicited by PDGF-BB, Akt activation was attenuated when PDGF-BB was co-administrated with atorvastatin calcium. In conclusion, atorvastatin calcium inhibits phenotype modulation of PDGF-BB-induced VSMCs and activation of the Akt signaling pathway, indicating that Akt might play a vital role in the modulation of phenotype. |
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In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high expression of contractile marker proteins. After injury to the vessel, VSMC shifts from a contractile phenotype to a pathological synthetic phenotype, associated with increased proliferation, migration and matrix secretion. It has been demonstrated that PDGF-BB is a critical mediator of VSMCs phenotypic switch. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methyl-glutaryl l coenzyme A (HMG-CoA) reductase, exhibits various protective effects against VSMCs. In this study, we investigated the effects of atorvastatin calcium on phenotype modulation of PDGF-BB-induced VSMCs and the related intracellular signal transduction pathways. Treatment of VSMCs with atorvastatin calcium showed dose-dependent inhibition of PDGF-BB-induced proliferation. Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs. Although Akt phosphorylation was strongly elicited by PDGF-BB, Akt activation was attenuated when PDGF-BB was co-administrated with atorvastatin calcium. In conclusion, atorvastatin calcium inhibits phenotype modulation of PDGF-BB-induced VSMCs and activation of the Akt signaling pathway, indicating that Akt might play a vital role in the modulation of phenotype.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0122577</identifier><identifier>PMID: 25874930</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actin ; Actin Cytoskeleton - drug effects ; Actin Cytoskeleton - metabolism ; Activation ; AKT protein ; Animals ; Antilipemic agents ; Atorvastatin ; Atorvastatin - pharmacology ; Becaplermin ; Blotting, Western ; Calcium ; Calponin ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Shape - drug effects ; Cells, Cultured ; Cellular signal transduction ; Coenzyme A ; Cytoskeleton ; Cytoskeleton - drug effects ; Cytoskeleton - metabolism ; DNA - biosynthesis ; DNA - genetics ; Dose-Response Relationship, Drug ; Down-Regulation - drug effects ; Enzymes ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Male ; Microscopy, Confocal ; Modulation ; Muscle contraction ; Muscle proteins ; Muscle, Smooth, Vascular - cytology ; Muscles ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Phenotypic plasticity ; Phosphorylation ; Platelet-derived growth factor ; Platelet-derived growth factor BB ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-sis - pharmacology ; Rats, Sprague-Dawley ; Reductase ; Secretion ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Smooth muscle ; Time Factors ; Vascular diseases</subject><ispartof>PloS one, 2015-04, Vol.10 (4), p.e0122577-e0122577</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Chen 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>2015 Chen et al 2015 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-1e6b99a5bb109840ab8407e9c6fa38af04233f9f66e707e13de347cc33ce03f83</citedby><cites>FETCH-LOGICAL-c692t-1e6b99a5bb109840ab8407e9c6fa38af04233f9f66e707e13de347cc33ce03f83</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/PMC4398430/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398430/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25874930$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Shuang</creatorcontrib><creatorcontrib>Liu, Baoqin</creatorcontrib><creatorcontrib>Kong, Dehui</creatorcontrib><creatorcontrib>Li, Si</creatorcontrib><creatorcontrib>Li, Chao</creatorcontrib><creatorcontrib>Wang, Huaqin</creatorcontrib><creatorcontrib>Sun, Yingxian</creatorcontrib><title>Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Plasticity of vascular smooth muscle cells (VSMCs) plays a central role in the onset and progression of proliferative vascular diseases. In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high expression of contractile marker proteins. After injury to the vessel, VSMC shifts from a contractile phenotype to a pathological synthetic phenotype, associated with increased proliferation, migration and matrix secretion. It has been demonstrated that PDGF-BB is a critical mediator of VSMCs phenotypic switch. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methyl-glutaryl l coenzyme A (HMG-CoA) reductase, exhibits various protective effects against VSMCs. In this study, we investigated the effects of atorvastatin calcium on phenotype modulation of PDGF-BB-induced VSMCs and the related intracellular signal transduction pathways. Treatment of VSMCs with atorvastatin calcium showed dose-dependent inhibition of PDGF-BB-induced proliferation. Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs. Although Akt phosphorylation was strongly elicited by PDGF-BB, Akt activation was attenuated when PDGF-BB was co-administrated with atorvastatin calcium. In conclusion, atorvastatin calcium inhibits phenotype modulation of PDGF-BB-induced VSMCs and activation of the Akt signaling pathway, indicating that Akt might play a vital role in the modulation of phenotype.</description><subject>Actin</subject><subject>Actin Cytoskeleton - drug effects</subject><subject>Actin Cytoskeleton - metabolism</subject><subject>Activation</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antilipemic agents</subject><subject>Atorvastatin</subject><subject>Atorvastatin - pharmacology</subject><subject>Becaplermin</subject><subject>Blotting, Western</subject><subject>Calcium</subject><subject>Calponin</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Shape - drug effects</subject><subject>Cells, Cultured</subject><subject>Cellular signal transduction</subject><subject>Coenzyme A</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - drug effects</subject><subject>Cytoskeleton - metabolism</subject><subject>DNA - biosynthesis</subject><subject>DNA - genetics</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation - drug effects</subject><subject>Enzymes</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>Male</subject><subject>Microscopy, Confocal</subject><subject>Modulation</subject><subject>Muscle contraction</subject><subject>Muscle proteins</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscles</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Phenotypic plasticity</subject><subject>Phosphorylation</subject><subject>Platelet-derived growth factor</subject><subject>Platelet-derived growth factor BB</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-sis - pharmacology</subject><subject>Rats, Sprague-Dawley</subject><subject>Reductase</subject><subject>Secretion</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Smooth muscle</subject><subject>Time Factors</subject><subject>Vascular diseases</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBYQkJwkWLHqZPcTOoKG5WGhhjs1nIcO3FJ7BA7HeXX46zp1KBdIEtxdPKc93zknCB4ieAM4QR9WJu-06yetUaLGURRNE-SR8ExynAUkgjixwfvR8Eza9cQznFKyNPgKJqnSZxheBz8WTjTbZh1zCkNOKu56hugdKVy5SxoK6GN27aKg8YUfe0po4GR4OvHi_Pw7CxUuui5KMDN9ZelBRvFQGFuddiJcg-7SoDFTwesKn26SpegZa66ZdvnwRPJaitejPdJ8OP80_fl5_Dy6mK1XFyGnGSRC5EgeZaxeZ4jmKUxZLl_JCLjRDKcMgnjCGOZSUJE4u0IFwLHCecYcwGxTPFJ8Hqn29bG0rFtliKSYJykOIGeWO2IwrA1bTvVsG5LDVP0zmC6krLOKV4LmsaM5EmeZyKWMUmjNIIRRAJznhYyxshrnY7R-rwRBRfadayeiE6_aFXR0mxojH11eEjm3SjQmV-9sI42ynJR10wL09_lHZMMEThU9uYf9OHqRqpkvgClpfFx-SBKF7GfGkKiFHtq9gDlTyEaxf2MSeXtE4f3EwfPOPHblay3lq6uv_0_e3UzZd8esJVgtausqfthmOwUjHcg74y1nZD3TUaQDiuy7wYdVoSOK-LdXh3-oHun_U7gvxk4DFI</recordid><startdate>20150415</startdate><enddate>20150415</enddate><creator>Chen, Shuang</creator><creator>Liu, Baoqin</creator><creator>Kong, Dehui</creator><creator>Li, Si</creator><creator>Li, Chao</creator><creator>Wang, Huaqin</creator><creator>Sun, Yingxian</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></search><sort><creationdate>20150415</creationdate><title>Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway</title><author>Chen, Shuang ; Liu, Baoqin ; Kong, Dehui ; Li, Si ; Li, Chao ; Wang, Huaqin ; Sun, Yingxian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-1e6b99a5bb109840ab8407e9c6fa38af04233f9f66e707e13de347cc33ce03f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Actin</topic><topic>Actin Cytoskeleton - drug effects</topic><topic>Actin Cytoskeleton - metabolism</topic><topic>Activation</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Antilipemic agents</topic><topic>Atorvastatin</topic><topic>Atorvastatin - pharmacology</topic><topic>Becaplermin</topic><topic>Blotting, Western</topic><topic>Calcium</topic><topic>Calponin</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Shape - drug effects</topic><topic>Cells, Cultured</topic><topic>Cellular signal transduction</topic><topic>Coenzyme A</topic><topic>Cytoskeleton</topic><topic>Cytoskeleton - drug effects</topic><topic>Cytoskeleton - metabolism</topic><topic>DNA - biosynthesis</topic><topic>DNA - genetics</topic><topic>Dose-Response Relationship, Drug</topic><topic>Down-Regulation - drug effects</topic><topic>Enzymes</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</topic><topic>Male</topic><topic>Microscopy, Confocal</topic><topic>Modulation</topic><topic>Muscle contraction</topic><topic>Muscle proteins</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscles</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Phenotypic plasticity</topic><topic>Phosphorylation</topic><topic>Platelet-derived growth factor</topic><topic>Platelet-derived growth factor BB</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-sis - pharmacology</topic><topic>Rats, Sprague-Dawley</topic><topic>Reductase</topic><topic>Secretion</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Smooth muscle</topic><topic>Time Factors</topic><topic>Vascular diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Shuang</creatorcontrib><creatorcontrib>Liu, Baoqin</creatorcontrib><creatorcontrib>Kong, Dehui</creatorcontrib><creatorcontrib>Li, Si</creatorcontrib><creatorcontrib>Li, Chao</creatorcontrib><creatorcontrib>Wang, Huaqin</creatorcontrib><creatorcontrib>Sun, Yingxian</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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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>Chen, Shuang</au><au>Liu, Baoqin</au><au>Kong, Dehui</au><au>Li, Si</au><au>Li, Chao</au><au>Wang, Huaqin</au><au>Sun, Yingxian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-04-15</date><risdate>2015</risdate><volume>10</volume><issue>4</issue><spage>e0122577</spage><epage>e0122577</epage><pages>e0122577-e0122577</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Plasticity of vascular smooth muscle cells (VSMCs) plays a central role in the onset and progression of proliferative vascular diseases. In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high expression of contractile marker proteins. After injury to the vessel, VSMC shifts from a contractile phenotype to a pathological synthetic phenotype, associated with increased proliferation, migration and matrix secretion. It has been demonstrated that PDGF-BB is a critical mediator of VSMCs phenotypic switch. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methyl-glutaryl l coenzyme A (HMG-CoA) reductase, exhibits various protective effects against VSMCs. In this study, we investigated the effects of atorvastatin calcium on phenotype modulation of PDGF-BB-induced VSMCs and the related intracellular signal transduction pathways. Treatment of VSMCs with atorvastatin calcium showed dose-dependent inhibition of PDGF-BB-induced proliferation. Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs. Although Akt phosphorylation was strongly elicited by PDGF-BB, Akt activation was attenuated when PDGF-BB was co-administrated with atorvastatin calcium. In conclusion, atorvastatin calcium inhibits phenotype modulation of PDGF-BB-induced VSMCs and activation of the Akt signaling pathway, indicating that Akt might play a vital role in the modulation of phenotype.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25874930</pmid><doi>10.1371/journal.pone.0122577</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1673378370 |
| 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 | Actin Actin Cytoskeleton - drug effects Actin Cytoskeleton - metabolism Activation AKT protein Animals Antilipemic agents Atorvastatin Atorvastatin - pharmacology Becaplermin Blotting, Western Calcium Calponin Cell Movement - drug effects Cell Proliferation - drug effects Cell Shape - drug effects Cells, Cultured Cellular signal transduction Coenzyme A Cytoskeleton Cytoskeleton - drug effects Cytoskeleton - metabolism DNA - biosynthesis DNA - genetics Dose-Response Relationship, Drug Down-Regulation - drug effects Enzymes Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Male Microscopy, Confocal Modulation Muscle contraction Muscle proteins Muscle, Smooth, Vascular - cytology Muscles Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Phenotypic plasticity Phosphorylation Platelet-derived growth factor Platelet-derived growth factor BB Proteins Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-sis - pharmacology Rats, Sprague-Dawley Reductase Secretion Signal transduction Signal Transduction - drug effects Signaling Smooth muscle Time Factors Vascular diseases |
| title | Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T03%3A34%3A09IST&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=Atorvastatin%20calcium%20inhibits%20phenotypic%20modulation%20of%20PDGF-BB-induced%20VSMCs%20via%20down-regulation%20the%20Akt%20signaling%20pathway&rft.jtitle=PloS%20one&rft.au=Chen,%20Shuang&rft.date=2015-04-15&rft.volume=10&rft.issue=4&rft.spage=e0122577&rft.epage=e0122577&rft.pages=e0122577-e0122577&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0122577&rft_dat=%3Cgale_plos_%3EA425766283%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=1673378370&rft_id=info:pmid/25874930&rft_galeid=A425766283&rft_doaj_id=oai_doaj_org_article_84a6b7bb9e4f4682820201e3cc8df431&rfr_iscdi=true |