Discoidin domain receptor 1 regulates bronchial epithelial repair and matrix metalloproteinase production
Discoidin domain receptor (DDR)1 is an extracellular matrix (ECM)-sensing receptor tyrosine kinase, which is activated by collagen and expressed in bronchial epithelium. DDR1 is responsible for maintaining the normal structure of skin and kidney epithelia and we hypothesised that DDR1 plays a regula...
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| Veröffentlicht in: | The European respiratory journal 2011-06, Vol.37 (6), p.1482-1493 |
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| container_title | The European respiratory journal |
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| creator | ROBERTS, M. E MAGOWAN, L HALL, I. P JOHNSON, S. R |
| description | Discoidin domain receptor (DDR)1 is an extracellular matrix (ECM)-sensing receptor tyrosine kinase, which is activated by collagen and expressed in bronchial epithelium. DDR1 is responsible for maintaining the normal structure of skin and kidney epithelia and we hypothesised that DDR1 plays a regulatory role in bronchial epithelial integrity by transducing signals from the airway ECM. Effects of DDR1 depletion were studied using RNA interference in primary human bronchial epithelial cells (HBECs) and BEAS-2B cells. The effects of overexpression of DDR1a and DDR1b in BEAS-2B cells were studied using a plasmid vector. We measured the effects on epithelial repair using a scratch wounding model, and levels of matrix metalloproteinases (MMPs) by gelatin zymography (MMP-2 and -9) and ELISA (MMP-7). We showed that knockdown of DDR1 slowed epithelial repair by 50%, which was associated with a reduction in levels of MMP-7, whilst DDR1 overexpression enhanced epithelial repair. DDR1 knockdown reduced proliferation of HBECs, but had no significant effect on adhesion to collagen I or other matrix substrates. These data suggest that ECM signalling via DDR1 regulates aspects of bronchial epithelial repair, integrity and MMP expression in the airways. |
| doi_str_mv | 10.1183/09031936.00039710 |
| format | Article |
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We showed that knockdown of DDR1 slowed epithelial repair by 50%, which was associated with a reduction in levels of MMP-7, whilst DDR1 overexpression enhanced epithelial repair. DDR1 knockdown reduced proliferation of HBECs, but had no significant effect on adhesion to collagen I or other matrix substrates. 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E</creatorcontrib><creatorcontrib>MAGOWAN, L</creatorcontrib><creatorcontrib>HALL, I. P</creatorcontrib><creatorcontrib>JOHNSON, S. R</creatorcontrib><title>Discoidin domain receptor 1 regulates bronchial epithelial repair and matrix metalloproteinase production</title><title>The European respiratory journal</title><addtitle>Eur Respir J</addtitle><description>Discoidin domain receptor (DDR)1 is an extracellular matrix (ECM)-sensing receptor tyrosine kinase, which is activated by collagen and expressed in bronchial epithelium. DDR1 is responsible for maintaining the normal structure of skin and kidney epithelia and we hypothesised that DDR1 plays a regulatory role in bronchial epithelial integrity by transducing signals from the airway ECM. Effects of DDR1 depletion were studied using RNA interference in primary human bronchial epithelial cells (HBECs) and BEAS-2B cells. The effects of overexpression of DDR1a and DDR1b in BEAS-2B cells were studied using a plasmid vector. We measured the effects on epithelial repair using a scratch wounding model, and levels of matrix metalloproteinases (MMPs) by gelatin zymography (MMP-2 and -9) and ELISA (MMP-7). We showed that knockdown of DDR1 slowed epithelial repair by 50%, which was associated with a reduction in levels of MMP-7, whilst DDR1 overexpression enhanced epithelial repair. DDR1 knockdown reduced proliferation of HBECs, but had no significant effect on adhesion to collagen I or other matrix substrates. These data suggest that ECM signalling via DDR1 regulates aspects of bronchial epithelial repair, integrity and MMP expression in the airways.</description><subject>Adult</subject><subject>Aged</subject><subject>Asthma - enzymology</subject><subject>Asthma - pathology</subject><subject>Biological and medical sciences</subject><subject>Bronchi - metabolism</subject><subject>Bronchi - pathology</subject><subject>Cell Adhesion</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Collagen Type I - metabolism</subject><subject>Discoidin Domain Receptor 1</subject><subject>Female</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 7 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pneumology</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Smoking - metabolism</subject><subject>Wound Healing</subject><subject>Young Adult</subject><issn>0903-1936</issn><issn>1399-3003</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkUFP3DAQha0KVJZtf0AvKBfUU8ATJ7FzRNsWkFbiAudo4kyKkRMH25Hg3-PV7sLF80b-5o38zNgv4FcASlzzhgtoRH3FOReNBP6NrUA0TS5Sf8JWu_t8B5yx8xBeOIe6FPCdnRVcqVKWsGLmjwnamd5MWe9GTMWTpjk6n0GS_xeLkULWeTfpZ4M2o9nEZ7I76WlG4zOc-mzE6M1bNlJEa93sXSQzYaAsyX7R0bjpBzsd0Ab6eahr9vTv7-PmLt8-3N5vbra5LkUT8yKdsgBFva5IoJLQKS0H0REM1EOJBVSAgrQkIKVAamgq3dVlV9UV70ms2e-9b1r9ulCI7ZieSNbiRG4JrZK8aKpaFYmEPam9C8HT0M7ejOjfW-DtLuD2GHB7DDjNXBzcl26k_nPimGgCLg8ABo128DhpE764sihk-gXxAYhthJo</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>ROBERTS, M. E</creator><creator>MAGOWAN, L</creator><creator>HALL, I. P</creator><creator>JOHNSON, S. R</creator><general>Maney</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>20110601</creationdate><title>Discoidin domain receptor 1 regulates bronchial epithelial repair and matrix metalloproteinase production</title><author>ROBERTS, M. E ; MAGOWAN, L ; HALL, I. P ; JOHNSON, S. R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-24397218edc5e3a871b8c7f3be1fed14a2151a3ec7e1e8817c195cb64b5650de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Asthma - enzymology</topic><topic>Asthma - pathology</topic><topic>Biological and medical sciences</topic><topic>Bronchi - metabolism</topic><topic>Bronchi - pathology</topic><topic>Cell Adhesion</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Collagen Type I - metabolism</topic><topic>Discoidin Domain Receptor 1</topic><topic>Female</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Male</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 7 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pneumology</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Smoking - metabolism</topic><topic>Wound Healing</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ROBERTS, M. E</creatorcontrib><creatorcontrib>MAGOWAN, L</creatorcontrib><creatorcontrib>HALL, I. P</creatorcontrib><creatorcontrib>JOHNSON, S. R</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>The European respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ROBERTS, M. E</au><au>MAGOWAN, L</au><au>HALL, I. P</au><au>JOHNSON, S. 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The effects of overexpression of DDR1a and DDR1b in BEAS-2B cells were studied using a plasmid vector. We measured the effects on epithelial repair using a scratch wounding model, and levels of matrix metalloproteinases (MMPs) by gelatin zymography (MMP-2 and -9) and ELISA (MMP-7). We showed that knockdown of DDR1 slowed epithelial repair by 50%, which was associated with a reduction in levels of MMP-7, whilst DDR1 overexpression enhanced epithelial repair. DDR1 knockdown reduced proliferation of HBECs, but had no significant effect on adhesion to collagen I or other matrix substrates. These data suggest that ECM signalling via DDR1 regulates aspects of bronchial epithelial repair, integrity and MMP expression in the airways.</abstract><cop>Leeds</cop><pub>Maney</pub><pmid>20884741</pmid><doi>10.1183/09031936.00039710</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Aged Asthma - enzymology Asthma - pathology Biological and medical sciences Bronchi - metabolism Bronchi - pathology Cell Adhesion Cell Line Cell Proliferation Cells, Cultured Collagen Type I - metabolism Discoidin Domain Receptor 1 Female Gene Knockdown Techniques Humans Male Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 7 - metabolism Matrix Metalloproteinase 9 - metabolism Medical sciences Middle Aged Pneumology Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Smoking - metabolism Wound Healing Young Adult |
| title | Discoidin domain receptor 1 regulates bronchial epithelial repair and matrix metalloproteinase production |
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