MMP7 Shedding of Syndecan-1 Facilitates Re-Epithelialization by Affecting α2β1 Integrin Activation
Background Lung injury promotes the expression of matrix metalloproteinase-7 (MMP7, matrilysin), which is required for neutrophil recruitment and re-epithelialization. MMP7 governs the lung inflammatory response through the shedding of syndecan-1. Because inflammation and repair are related events,...
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| Veröffentlicht in: | PloS one 2009-08, Vol.4 (8), p.e6565 |
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| creator | Chen, Peter Abacherli, Laura E. Nadler, Samuel T. Wang, Ying Li, Qinglang Parks, William C. |
| description | Background Lung injury promotes the expression of matrix metalloproteinase-7 (MMP7, matrilysin), which is required for neutrophil recruitment and re-epithelialization. MMP7 governs the lung inflammatory response through the shedding of syndecan-1. Because inflammation and repair are related events, we evaluated the role of syndecan-1 shedding in lung re-epithelialization. Methodology/Principal Finding Epithelial injury induced syndecan-1 shedding from wild-type epithelium but not from Mmp7−/− mice in vitro and in vivo. Moreover, cell migration and wound closure was enhanced by MMP7 shedding of syndecan-1. Additionally, we found that syndecan-1 augmented cell adhesion to collagen by controlling the affinity state of the α2β1 integrin. Conclusion/Significance MMP7 shedding of syndecan-1 facilitates wound closure by causing the α2β1 integrin to assume a less active conformation thereby removing restrictions to migration. MMP7 acts in the lungs to regulate inflammation and repair, and our data now show that both these functions are controlled through the shedding of syndecan-1. |
| doi_str_mv | 10.1371/journal.pone.0006565 |
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MMP7 governs the lung inflammatory response through the shedding of syndecan-1. Because inflammation and repair are related events, we evaluated the role of syndecan-1 shedding in lung re-epithelialization. Methodology/Principal Finding Epithelial injury induced syndecan-1 shedding from wild-type epithelium but not from Mmp7−/− mice in vitro and in vivo. Moreover, cell migration and wound closure was enhanced by MMP7 shedding of syndecan-1. Additionally, we found that syndecan-1 augmented cell adhesion to collagen by controlling the affinity state of the α2β1 integrin. Conclusion/Significance MMP7 shedding of syndecan-1 facilitates wound closure by causing the α2β1 integrin to assume a less active conformation thereby removing restrictions to migration. MMP7 acts in the lungs to regulate inflammation and repair, and our data now show that both these functions are controlled through the shedding of syndecan-1.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0006565</identifier><identifier>PMID: 19668337</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Arteriosclerosis ; Cell adhesion ; Cell adhesion & migration ; Cell Biology ; Cell Biology/Cell Adhesion ; Cell Biology/Extra-Cellular Matrix ; Cell migration ; Collagen ; Conformation ; Epithelium ; Fibroblasts ; Heparan sulfate ; Inflammation ; Inflammatory response ; Leukocyte migration ; Ligands ; Lungs ; Matrilysin ; Matrix metalloproteinase ; Medicine ; Metalloproteinase ; Microscopy ; Molecular biology ; Phosphorylation ; Recruitment ; Repair ; Rodents ; Shedding ; Syndecan ; Thrombosis ; Wound healing ; Wounds</subject><ispartof>PloS one, 2009-08, Vol.4 (8), p.e6565</ispartof><rights>2009 Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (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>Chen et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3855-b1d938b5f7cfc30378e355f9d5595ee296ae312ca6a3e5e155357c6a19079153</citedby><cites>FETCH-LOGICAL-c3855-b1d938b5f7cfc30378e355f9d5595ee296ae312ca6a3e5e155357c6a19079153</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/PMC2719060/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719060/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2929,23871,27929,27930,53796,53798</link.rule.ids></links><search><contributor>Vij, Neeraj</contributor><creatorcontrib>Chen, Peter</creatorcontrib><creatorcontrib>Abacherli, Laura E.</creatorcontrib><creatorcontrib>Nadler, Samuel T.</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Li, Qinglang</creatorcontrib><creatorcontrib>Parks, William C.</creatorcontrib><title>MMP7 Shedding of Syndecan-1 Facilitates Re-Epithelialization by Affecting α2β1 Integrin Activation</title><title>PloS one</title><description>Background Lung injury promotes the expression of matrix metalloproteinase-7 (MMP7, matrilysin), which is required for neutrophil recruitment and re-epithelialization. MMP7 governs the lung inflammatory response through the shedding of syndecan-1. Because inflammation and repair are related events, we evaluated the role of syndecan-1 shedding in lung re-epithelialization. Methodology/Principal Finding Epithelial injury induced syndecan-1 shedding from wild-type epithelium but not from Mmp7−/− mice in vitro and in vivo. Moreover, cell migration and wound closure was enhanced by MMP7 shedding of syndecan-1. Additionally, we found that syndecan-1 augmented cell adhesion to collagen by controlling the affinity state of the α2β1 integrin. Conclusion/Significance MMP7 shedding of syndecan-1 facilitates wound closure by causing the α2β1 integrin to assume a less active conformation thereby removing restrictions to migration. MMP7 acts in the lungs to regulate inflammation and repair, and our data now show that both these functions are controlled through the shedding of syndecan-1.</description><subject>Arteriosclerosis</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell Biology/Cell Adhesion</subject><subject>Cell Biology/Extra-Cellular Matrix</subject><subject>Cell migration</subject><subject>Collagen</subject><subject>Conformation</subject><subject>Epithelium</subject><subject>Fibroblasts</subject><subject>Heparan sulfate</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Leukocyte migration</subject><subject>Ligands</subject><subject>Lungs</subject><subject>Matrilysin</subject><subject>Matrix metalloproteinase</subject><subject>Medicine</subject><subject>Metalloproteinase</subject><subject>Microscopy</subject><subject>Molecular biology</subject><subject>Phosphorylation</subject><subject>Recruitment</subject><subject>Repair</subject><subject>Rodents</subject><subject>Shedding</subject><subject>Syndecan</subject><subject>Thrombosis</subject><subject>Wound 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Shedding of Syndecan-1 Facilitates Re-Epithelialization by Affecting α2β1 Integrin Activation</title><author>Chen, Peter ; Abacherli, Laura E. ; Nadler, Samuel T. ; Wang, Ying ; Li, Qinglang ; Parks, William C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3855-b1d938b5f7cfc30378e355f9d5595ee296ae312ca6a3e5e155357c6a19079153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Arteriosclerosis</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cell Biology/Cell Adhesion</topic><topic>Cell Biology/Extra-Cellular Matrix</topic><topic>Cell migration</topic><topic>Collagen</topic><topic>Conformation</topic><topic>Epithelium</topic><topic>Fibroblasts</topic><topic>Heparan sulfate</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Leukocyte 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Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Peter</au><au>Abacherli, Laura E.</au><au>Nadler, Samuel T.</au><au>Wang, Ying</au><au>Li, Qinglang</au><au>Parks, William C.</au><au>Vij, Neeraj</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MMP7 Shedding of Syndecan-1 Facilitates Re-Epithelialization by Affecting α2β1 Integrin Activation</atitle><jtitle>PloS one</jtitle><date>2009-08-10</date><risdate>2009</risdate><volume>4</volume><issue>8</issue><spage>e6565</spage><pages>e6565-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Background Lung injury promotes the expression of matrix metalloproteinase-7 (MMP7, matrilysin), which is required for neutrophil recruitment and re-epithelialization. MMP7 governs the lung inflammatory response through the shedding of syndecan-1. Because inflammation and repair are related events, we evaluated the role of syndecan-1 shedding in lung re-epithelialization. Methodology/Principal Finding Epithelial injury induced syndecan-1 shedding from wild-type epithelium but not from Mmp7−/− mice in vitro and in vivo. Moreover, cell migration and wound closure was enhanced by MMP7 shedding of syndecan-1. Additionally, we found that syndecan-1 augmented cell adhesion to collagen by controlling the affinity state of the α2β1 integrin. Conclusion/Significance MMP7 shedding of syndecan-1 facilitates wound closure by causing the α2β1 integrin to assume a less active conformation thereby removing restrictions to migration. MMP7 acts in the lungs to regulate inflammation and repair, and our data now show that both these functions are controlled through the shedding of syndecan-1.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>19668337</pmid><doi>10.1371/journal.pone.0006565</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Arteriosclerosis Cell adhesion Cell adhesion & migration Cell Biology Cell Biology/Cell Adhesion Cell Biology/Extra-Cellular Matrix Cell migration Collagen Conformation Epithelium Fibroblasts Heparan sulfate Inflammation Inflammatory response Leukocyte migration Ligands Lungs Matrilysin Matrix metalloproteinase Medicine Metalloproteinase Microscopy Molecular biology Phosphorylation Recruitment Repair Rodents Shedding Syndecan Thrombosis Wound healing Wounds |
| title | MMP7 Shedding of Syndecan-1 Facilitates Re-Epithelialization by Affecting α2β1 Integrin Activation |
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