A disintegrin and metalloenzyme (ADAM) 17 activation is regulated by α5β1 integrin in kidney mesangial cells
The disintegrin and metalloenzyme ADAM17 participates in numerous inflammatory and proliferative diseases, and its pathophysiological role was implicated in kidney fibrosis, polycystic kidney disease and other chronic kidney diseases. At present, we have little understanding how the enzyme activity...
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| Veröffentlicht in: | PloS one 2012-03, Vol.7 (3), p.e33350-e33350 |
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| creator | Gooz, Pal Dang, Yujing Higashiyama, Shigeki Twal, Waleed O Haycraft, Courtney J Gooz, Monika |
| description | The disintegrin and metalloenzyme ADAM17 participates in numerous inflammatory and proliferative diseases, and its pathophysiological role was implicated in kidney fibrosis, polycystic kidney disease and other chronic kidney diseases. At present, we have little understanding how the enzyme activity is regulated. In this study we wanted to characterize the role of α5β1 integrin in ADAM17 activity regulation during G protein-coupled receptor (GPCR) stimulation.
We showed previously that the profibrotic GPCR agonist serotonin (5-HT) induced kidney mesangial cell proliferation through ADAM17 activation and heparin-binding epidermal growth factor (HB-EGF) shedding. In the present studies we observed that in unstimulated mesangial cell lysates α5β1 integrin co-precipitated with ADAM17 and that 5-HT treatment of the cells induced dissociation of α5β1 integrin from ADAM17. Using fluorescence immunostaining and in situ proximity ligation assay, we identified the perinuclear region as the localization of the ADAM17/α5β1 integrin interaction. In cell-free assays, we showed that purified α5β1 integrin and β1 integrin dose-dependently bound to and inhibited activity of recombinant ADAM17. We provided evidence that the conformation of the integrin determines its ADAM17-binding ability. To study the effect of β1 integrin on ADAM17 sheddase activity, we employed alkaline phosphatase-tagged HB-EGF. Overexpression of β1 integrin lead to complete inhibition of 5-HT-induced HB-EGF shedding and silencing β1 integrin by siRNA significantly increased mesangial cells ADAM17 responsiveness to 5-HT.
Our data show for the first time that β1 integrin has an important physiological role in ADAM17 activity regulation. We suggest that regulating α5β1 integrin binding to ADAM17 could be an attractive therapeutic target in chronic kidney diseases. |
| doi_str_mv | 10.1371/journal.pone.0033350 |
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We showed previously that the profibrotic GPCR agonist serotonin (5-HT) induced kidney mesangial cell proliferation through ADAM17 activation and heparin-binding epidermal growth factor (HB-EGF) shedding. In the present studies we observed that in unstimulated mesangial cell lysates α5β1 integrin co-precipitated with ADAM17 and that 5-HT treatment of the cells induced dissociation of α5β1 integrin from ADAM17. Using fluorescence immunostaining and in situ proximity ligation assay, we identified the perinuclear region as the localization of the ADAM17/α5β1 integrin interaction. In cell-free assays, we showed that purified α5β1 integrin and β1 integrin dose-dependently bound to and inhibited activity of recombinant ADAM17. We provided evidence that the conformation of the integrin determines its ADAM17-binding ability. To study the effect of β1 integrin on ADAM17 sheddase activity, we employed alkaline phosphatase-tagged HB-EGF. Overexpression of β1 integrin lead to complete inhibition of 5-HT-induced HB-EGF shedding and silencing β1 integrin by siRNA significantly increased mesangial cells ADAM17 responsiveness to 5-HT.
Our data show for the first time that β1 integrin has an important physiological role in ADAM17 activity regulation. We suggest that regulating α5β1 integrin binding to ADAM17 could be an attractive therapeutic target in chronic kidney diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0033350</identifier><identifier>PMID: 22413019</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; ADAM Proteins - metabolism ; ADAM17 Protein ; Alkaline phosphatase ; Angiogenesis ; Animals ; Apoptosis ; Binding ; Biochemistry ; Biology ; Breast cancer ; Cell activation ; Cell adhesion & migration ; Cell growth ; Cell proliferation ; Cells, Cultured ; Diseases ; Dissociation ; Enzymatic activity ; Enzyme Activation ; Enzyme activity ; Enzymes ; Epidermal growth factor ; Fibrosis ; Fluorescence ; G protein-coupled receptors ; Heparin ; Heparin-binding EGF-like Growth Factor ; Inflammation ; Inhibition ; Integrin alpha5beta1 - metabolism ; Integrin beta1 - metabolism ; Intercellular Signaling Peptides and Proteins - metabolism ; Kidney diseases ; Kinases ; Ligands ; Localization ; Lysates ; Medicine ; Mesangial cells ; Mesangial Cells - enzymology ; Mesangial Cells - metabolism ; Multiprotein Complexes - metabolism ; Permeability ; Polycystic kidney ; Protein Binding - drug effects ; Protein Transport ; Proteins ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled - agonists ; Rodents ; Serotonin ; Shedding ; siRNA ; Thiophenes - pharmacology ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2012-03, Vol.7 (3), p.e33350-e33350</ispartof><rights>2012. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5060-d5c683158d68a9f4c1b8bc411b33a5c1218ca40e9cbcad87e89466c915e5b62d3</citedby><cites>FETCH-LOGICAL-c5060-d5c683158d68a9f4c1b8bc411b33a5c1218ca40e9cbcad87e89466c915e5b62d3</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/PMC3297637/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297637/$$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/22413019$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gooz, Pal</creatorcontrib><creatorcontrib>Dang, Yujing</creatorcontrib><creatorcontrib>Higashiyama, Shigeki</creatorcontrib><creatorcontrib>Twal, Waleed O</creatorcontrib><creatorcontrib>Haycraft, Courtney J</creatorcontrib><creatorcontrib>Gooz, Monika</creatorcontrib><title>A disintegrin and metalloenzyme (ADAM) 17 activation is regulated by α5β1 integrin in kidney mesangial cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The disintegrin and metalloenzyme ADAM17 participates in numerous inflammatory and proliferative diseases, and its pathophysiological role was implicated in kidney fibrosis, polycystic kidney disease and other chronic kidney diseases. At present, we have little understanding how the enzyme activity is regulated. In this study we wanted to characterize the role of α5β1 integrin in ADAM17 activity regulation during G protein-coupled receptor (GPCR) stimulation.
We showed previously that the profibrotic GPCR agonist serotonin (5-HT) induced kidney mesangial cell proliferation through ADAM17 activation and heparin-binding epidermal growth factor (HB-EGF) shedding. In the present studies we observed that in unstimulated mesangial cell lysates α5β1 integrin co-precipitated with ADAM17 and that 5-HT treatment of the cells induced dissociation of α5β1 integrin from ADAM17. Using fluorescence immunostaining and in situ proximity ligation assay, we identified the perinuclear region as the localization of the ADAM17/α5β1 integrin interaction. In cell-free assays, we showed that purified α5β1 integrin and β1 integrin dose-dependently bound to and inhibited activity of recombinant ADAM17. We provided evidence that the conformation of the integrin determines its ADAM17-binding ability. To study the effect of β1 integrin on ADAM17 sheddase activity, we employed alkaline phosphatase-tagged HB-EGF. Overexpression of β1 integrin lead to complete inhibition of 5-HT-induced HB-EGF shedding and silencing β1 integrin by siRNA significantly increased mesangial cells ADAM17 responsiveness to 5-HT.
Our data show for the first time that β1 integrin has an important physiological role in ADAM17 activity regulation. We suggest that regulating α5β1 integrin binding to ADAM17 could be an attractive therapeutic target in chronic kidney diseases.</description><subject>Activation</subject><subject>ADAM Proteins - metabolism</subject><subject>ADAM17 Protein</subject><subject>Alkaline phosphatase</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Binding</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Breast cancer</subject><subject>Cell activation</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cells, Cultured</subject><subject>Diseases</subject><subject>Dissociation</subject><subject>Enzymatic activity</subject><subject>Enzyme Activation</subject><subject>Enzyme activity</subject><subject>Enzymes</subject><subject>Epidermal growth factor</subject><subject>Fibrosis</subject><subject>Fluorescence</subject><subject>G protein-coupled receptors</subject><subject>Heparin</subject><subject>Heparin-binding EGF-like Growth Factor</subject><subject>Inflammation</subject><subject>Inhibition</subject><subject>Integrin alpha5beta1 - metabolism</subject><subject>Integrin beta1 - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Kidney diseases</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Localization</subject><subject>Lysates</subject><subject>Medicine</subject><subject>Mesangial cells</subject><subject>Mesangial Cells - enzymology</subject><subject>Mesangial Cells - metabolism</subject><subject>Multiprotein Complexes - metabolism</subject><subject>Permeability</subject><subject>Polycystic kidney</subject><subject>Protein Binding - drug effects</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Rodents</subject><subject>Serotonin</subject><subject>Shedding</subject><subject>siRNA</subject><subject>Thiophenes - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkt-KEzEUxgdR3LX6BqIBL9SL1vyZZJIboaz_Fla80euQSc7U1EzSTWYW6lvpg-wzObXdsitCIIfk-37JOXxV9ZTgBWENebNOY44mLDYpwgJjxhjH96pTohidC4rZ_Vv1SfWolDXGnEkhHlYnlNaEYaJOq7hEzhcfB1hlH5GJDvUwmBASxJ_bHtCr5bvl59eINMjYwV-ZwaeIfEEZVmMwAzjUbtH1L379m6AjZlo_vIuwnWDFxJU3AVkIoTyuHnQmFHhy2GfVtw_vv559ml98-Xh-tryYW44FnjtuhWSESyekUV1tSStbWxPSMma4JZRIa2oMyrbWONmAVLUQVhEOvBXUsVn1fM_dhFT0YVRFE0ZrjLGkZFKc7xUumbXeZN-bvNXJeP33IOWVNnnwNoBuOhCcdMBMI-paMsWVpYwCJm3n6FTOqreH18a2B2chDtmEO9C7N9F_16t0pRlVjWDNBHh5AOR0OUIZdO_LbmAmQhqLVrRRUiq-U774R_n_5uq9yuZUSobu-BeC9S49Ny69S48-pGeyPbvdx9F0Exf2B0arw7U</recordid><startdate>20120308</startdate><enddate>20120308</enddate><creator>Gooz, Pal</creator><creator>Dang, Yujing</creator><creator>Higashiyama, Shigeki</creator><creator>Twal, Waleed O</creator><creator>Haycraft, Courtney J</creator><creator>Gooz, Monika</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>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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120308</creationdate><title>A disintegrin and metalloenzyme (ADAM) 17 activation is regulated by α5β1 integrin in kidney mesangial cells</title><author>Gooz, Pal ; Dang, Yujing ; Higashiyama, Shigeki ; Twal, Waleed O ; Haycraft, Courtney J ; Gooz, Monika</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5060-d5c683158d68a9f4c1b8bc411b33a5c1218ca40e9cbcad87e89466c915e5b62d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Activation</topic><topic>ADAM Proteins - metabolism</topic><topic>ADAM17 Protein</topic><topic>Alkaline phosphatase</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Binding</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Breast cancer</topic><topic>Cell activation</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cells, Cultured</topic><topic>Diseases</topic><topic>Dissociation</topic><topic>Enzymatic activity</topic><topic>Enzyme Activation</topic><topic>Enzyme activity</topic><topic>Enzymes</topic><topic>Epidermal growth factor</topic><topic>Fibrosis</topic><topic>Fluorescence</topic><topic>G protein-coupled receptors</topic><topic>Heparin</topic><topic>Heparin-binding EGF-like Growth Factor</topic><topic>Inflammation</topic><topic>Inhibition</topic><topic>Integrin alpha5beta1 - metabolism</topic><topic>Integrin beta1 - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Kidney diseases</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Localization</topic><topic>Lysates</topic><topic>Medicine</topic><topic>Mesangial cells</topic><topic>Mesangial Cells - enzymology</topic><topic>Mesangial Cells - metabolism</topic><topic>Multiprotein Complexes - metabolism</topic><topic>Permeability</topic><topic>Polycystic kidney</topic><topic>Protein Binding - drug effects</topic><topic>Protein Transport</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Rodents</topic><topic>Serotonin</topic><topic>Shedding</topic><topic>siRNA</topic><topic>Thiophenes - pharmacology</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gooz, Pal</creatorcontrib><creatorcontrib>Dang, Yujing</creatorcontrib><creatorcontrib>Higashiyama, Shigeki</creatorcontrib><creatorcontrib>Twal, Waleed O</creatorcontrib><creatorcontrib>Haycraft, Courtney J</creatorcontrib><creatorcontrib>Gooz, Monika</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</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>Gooz, Pal</au><au>Dang, Yujing</au><au>Higashiyama, Shigeki</au><au>Twal, Waleed O</au><au>Haycraft, Courtney J</au><au>Gooz, Monika</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A disintegrin and metalloenzyme (ADAM) 17 activation is regulated by α5β1 integrin in kidney mesangial cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-03-08</date><risdate>2012</risdate><volume>7</volume><issue>3</issue><spage>e33350</spage><epage>e33350</epage><pages>e33350-e33350</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The disintegrin and metalloenzyme ADAM17 participates in numerous inflammatory and proliferative diseases, and its pathophysiological role was implicated in kidney fibrosis, polycystic kidney disease and other chronic kidney diseases. At present, we have little understanding how the enzyme activity is regulated. In this study we wanted to characterize the role of α5β1 integrin in ADAM17 activity regulation during G protein-coupled receptor (GPCR) stimulation.
We showed previously that the profibrotic GPCR agonist serotonin (5-HT) induced kidney mesangial cell proliferation through ADAM17 activation and heparin-binding epidermal growth factor (HB-EGF) shedding. In the present studies we observed that in unstimulated mesangial cell lysates α5β1 integrin co-precipitated with ADAM17 and that 5-HT treatment of the cells induced dissociation of α5β1 integrin from ADAM17. Using fluorescence immunostaining and in situ proximity ligation assay, we identified the perinuclear region as the localization of the ADAM17/α5β1 integrin interaction. In cell-free assays, we showed that purified α5β1 integrin and β1 integrin dose-dependently bound to and inhibited activity of recombinant ADAM17. We provided evidence that the conformation of the integrin determines its ADAM17-binding ability. To study the effect of β1 integrin on ADAM17 sheddase activity, we employed alkaline phosphatase-tagged HB-EGF. Overexpression of β1 integrin lead to complete inhibition of 5-HT-induced HB-EGF shedding and silencing β1 integrin by siRNA significantly increased mesangial cells ADAM17 responsiveness to 5-HT.
Our data show for the first time that β1 integrin has an important physiological role in ADAM17 activity regulation. We suggest that regulating α5β1 integrin binding to ADAM17 could be an attractive therapeutic target in chronic kidney diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22413019</pmid><doi>10.1371/journal.pone.0033350</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Activation ADAM Proteins - metabolism ADAM17 Protein Alkaline phosphatase Angiogenesis Animals Apoptosis Binding Biochemistry Biology Breast cancer Cell activation Cell adhesion & migration Cell growth Cell proliferation Cells, Cultured Diseases Dissociation Enzymatic activity Enzyme Activation Enzyme activity Enzymes Epidermal growth factor Fibrosis Fluorescence G protein-coupled receptors Heparin Heparin-binding EGF-like Growth Factor Inflammation Inhibition Integrin alpha5beta1 - metabolism Integrin beta1 - metabolism Intercellular Signaling Peptides and Proteins - metabolism Kidney diseases Kinases Ligands Localization Lysates Medicine Mesangial cells Mesangial Cells - enzymology Mesangial Cells - metabolism Multiprotein Complexes - metabolism Permeability Polycystic kidney Protein Binding - drug effects Protein Transport Proteins Rats Rats, Sprague-Dawley Receptors, G-Protein-Coupled - agonists Rodents Serotonin Shedding siRNA Thiophenes - pharmacology Tumor necrosis factor-TNF |
| title | A disintegrin and metalloenzyme (ADAM) 17 activation is regulated by α5β1 integrin in kidney mesangial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T08%3A51%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20disintegrin%20and%20metalloenzyme%20(ADAM)%2017%20activation%20is%20regulated%20by%20%CE%B15%CE%B21%20integrin%20in%20kidney%20mesangial%20cells&rft.jtitle=PloS%20one&rft.au=Gooz,%20Pal&rft.date=2012-03-08&rft.volume=7&rft.issue=3&rft.spage=e33350&rft.epage=e33350&rft.pages=e33350-e33350&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0033350&rft_dat=%3Cproquest_plos_%3E2936964541%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1324000821&rft_id=info:pmid/22413019&rft_doaj_id=oai_doaj_org_article_7fe651fe3a764483959c232e01bfd2c2&rfr_iscdi=true |