Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation
Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum t...
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| Veröffentlicht in: | Journal of medical microbiology 2014-02, Vol.63 (2), p.155-161 |
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| container_title | Journal of medical microbiology |
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| creator | Zhang, Junxia Wang, Haiwei Zhang, Lijun Zhang, Tengteng Wang, Beibei Li, Xiankui Wei, Junyan |
| description | Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K. |
| doi_str_mv | 10.1099/jmm.0.065359-0 |
| format | Article |
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However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.</description><identifier>ISSN: 0022-2615</identifier><identifier>EISSN: 1473-5644</identifier><identifier>DOI: 10.1099/jmm.0.065359-0</identifier><identifier>PMID: 24248991</identifier><identifier>CODEN: JMMIAV</identifier><language>eng</language><publisher>Reading: Society for General Microbiology</publisher><subject>Animals ; Bacteriology ; Biological and medical sciences ; Cell Movement ; Cells, Cultured ; Chlamydophila pneumoniae - growth & development ; Fundamental and applied biological sciences. Psychology ; Infectious diseases ; Medical sciences ; Microbiology ; Miscellaneous ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - microbiology ; Myocytes, Smooth Muscle - physiology ; Phosphatidylinositol 3-Kinases - metabolism ; rac1 GTP-Binding Protein - metabolism ; Rats</subject><ispartof>Journal of medical microbiology, 2014-02, Vol.63 (2), p.155-161</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-13e0e9e0f3ac34171a6430c80817e8dd56d4ff08d75801c0316ba1d0179028413</citedby><cites>FETCH-LOGICAL-c325t-13e0e9e0f3ac34171a6430c80817e8dd56d4ff08d75801c0316ba1d0179028413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3746,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28351650$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24248991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Junxia</creatorcontrib><creatorcontrib>Wang, Haiwei</creatorcontrib><creatorcontrib>Zhang, Lijun</creatorcontrib><creatorcontrib>Zhang, Tengteng</creatorcontrib><creatorcontrib>Wang, Beibei</creatorcontrib><creatorcontrib>Li, Xiankui</creatorcontrib><creatorcontrib>Wei, Junyan</creatorcontrib><title>Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation</title><title>Journal of medical microbiology</title><addtitle>J Med Microbiol</addtitle><description>Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.</description><subject>Animals</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Cell Movement</subject><subject>Cells, Cultured</subject><subject>Chlamydophila pneumoniae - growth & development</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Infectious diseases</subject><subject>Medical sciences</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Myocytes, Smooth Muscle - microbiology</subject><subject>Myocytes, Smooth Muscle - physiology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>Rats</subject><issn>0022-2615</issn><issn>1473-5644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LxDAQhoMouq5ePUougpfWmSZpm6MsfsGCIHqO2SR1uzTt2mwX9t-b_VBPMwzPvMw8hFwhpAhS3i28TyGFXDAhEzgiI-QFS0TO-TEZAWRZkuUozsh5CAsALBiTp-Qs4xkvpcQR-ZzMG-03ttZ02brBd22tHa3byplV3bWxs4Nxga51MEOjexp8163m1A_BNI4a1zTU11-93tHrGPOmDVIdt9e72QU5qXQT3OWhjsnH48P75DmZvj69TO6niWGZWCXIHDjpoGLaMI4F6pwzMCWUWLjSWpFbXlVQ2kKUgAYY5jONNn4kISs5sjG53ecu--57cGGlfB225-nWdUNQyGVWAAKXEU33qOm7EHpXqWVfe91vFILaWlXRqgK1t6ogLlwfsoeZd_YP_9UYgZsDEDXppup1a-rwz5VMYC6A_QAmi4AR</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Zhang, Junxia</creator><creator>Wang, Haiwei</creator><creator>Zhang, Lijun</creator><creator>Zhang, Tengteng</creator><creator>Wang, Beibei</creator><creator>Li, Xiankui</creator><creator>Wei, Junyan</creator><general>Society for General Microbiology</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20140201</creationdate><title>Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation</title><author>Zhang, Junxia ; Wang, Haiwei ; Zhang, Lijun ; Zhang, Tengteng ; Wang, Beibei ; Li, Xiankui ; Wei, Junyan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-13e0e9e0f3ac34171a6430c80817e8dd56d4ff08d75801c0316ba1d0179028413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Cell Movement</topic><topic>Cells, Cultured</topic><topic>Chlamydophila pneumoniae - growth & development</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Infectious diseases</topic><topic>Medical sciences</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Myocytes, Smooth Muscle - microbiology</topic><topic>Myocytes, Smooth Muscle - physiology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>Rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Junxia</creatorcontrib><creatorcontrib>Wang, Haiwei</creatorcontrib><creatorcontrib>Zhang, Lijun</creatorcontrib><creatorcontrib>Zhang, Tengteng</creatorcontrib><creatorcontrib>Wang, Beibei</creatorcontrib><creatorcontrib>Li, Xiankui</creatorcontrib><creatorcontrib>Wei, Junyan</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of medical microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Junxia</au><au>Wang, Haiwei</au><au>Zhang, Lijun</au><au>Zhang, Tengteng</au><au>Wang, Beibei</au><au>Li, Xiankui</au><au>Wei, Junyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation</atitle><jtitle>Journal of medical microbiology</jtitle><addtitle>J Med Microbiol</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>63</volume><issue>2</issue><spage>155</spage><epage>161</epage><pages>155-161</pages><issn>0022-2615</issn><eissn>1473-5644</eissn><coden>JMMIAV</coden><abstract>Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.</abstract><cop>Reading</cop><pub>Society for General Microbiology</pub><pmid>24248991</pmid><doi>10.1099/jmm.0.065359-0</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Microbiology Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Bacteriology Biological and medical sciences Cell Movement Cells, Cultured Chlamydophila pneumoniae - growth & development Fundamental and applied biological sciences. Psychology Infectious diseases Medical sciences Microbiology Miscellaneous Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - microbiology Myocytes, Smooth Muscle - physiology Phosphatidylinositol 3-Kinases - metabolism rac1 GTP-Binding Protein - metabolism Rats |
| title | Chlamydia pneumoniae infection induces vascular smooth muscle cell migration via Rac1 activation |
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