An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis

Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal ren...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Pathology 1993, Vol.25 (4), p.327-332
Hauptverfasser: Roy-Chaudhury, Prabir, Jones, Michael C., Simpson, John G., Macleod, Alison M., Haites, Neva E., Power, David A.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 332
container_issue 4
container_start_page 327
container_title Pathology
container_volume 25
creator Roy-Chaudhury, Prabir
Jones, Michael C.
Simpson, John G.
Macleod, Alison M.
Haites, Neva E.
Power, David A.
description Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFRl), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.
doi_str_mv 10.3109/00313029309090851
format Article
fullrecord <record><control><sourceid>elsevier_cross</sourceid><recordid>TN_cdi_crossref_primary_10_3109_00313029309090851</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0031302516355684</els_id><sourcerecordid>S0031302516355684</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-aaae886992bd928e8f504cb0fb8d9687f9de6cb350a93f100916d976133f3d083</originalsourceid><addsrcrecordid>eNqNkM9KAzEQxoMoWKsP4C0vsJo0u9sET6X4Dwpe9LykyaSbspssSbbak69uSgUPgsgcZpiZ72Pmh9A1JTeMEnFLCKOMzAQjIgev6Ama0LKuCiYYPUWTw7zIC9U5uohxSwgpOecT9Llw2Pb96HxrY_Kd31glOxzTqPfYGwyD1RD63NoE_55abKRKPuAACoZDIZ3GDsafBnwMAWK0Phs7PATfWQNBJrsDvOl8D2HsvIOhDTbZeInOjOwiXH3nKXp7uH9dPhWrl8fn5WJVqLKcpUJKCZzXQszWWsw4cFORUq2JWXMtaj43QkOt1qwiUjBDCRG01mJeU8YM04SzKaJHXxV8jAFMMwTby7BvKGkOBJtfBLPm7qixzvjMoAXZpVbJAM3Wj8Hle_-jhvzWzkJoorLgFGibWaVGe_uH-guZyIyH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis</title><source>Taylor &amp; Francis</source><source>Alma/SFX Local Collection</source><creator>Roy-Chaudhury, Prabir ; Jones, Michael C. ; Simpson, John G. ; Macleod, Alison M. ; Haites, Neva E. ; Power, David A.</creator><creatorcontrib>Roy-Chaudhury, Prabir ; Jones, Michael C. ; Simpson, John G. ; Macleod, Alison M. ; Haites, Neva E. ; Power, David A.</creatorcontrib><description>Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFRl), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.</description><identifier>ISSN: 0031-3025</identifier><identifier>EISSN: 1465-3931</identifier><identifier>DOI: 10.3109/00313029309090851</identifier><language>eng</language><publisher>Elsevier B.V</publisher><subject>epidermal growth factor receptor ; glornerulonephritis ; immunohistochemistry ; Kidney ; proliferative</subject><ispartof>Pathology, 1993, Vol.25 (4), p.327-332</ispartof><rights>1993 Royal College of Pathologists of Australasia</rights><rights>1993 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 1993</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-aaae886992bd928e8f504cb0fb8d9687f9de6cb350a93f100916d976133f3d083</citedby><cites>FETCH-LOGICAL-c442t-aaae886992bd928e8f504cb0fb8d9687f9de6cb350a93f100916d976133f3d083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.3109/00313029309090851$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.3109/00313029309090851$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>314,776,780,4010,27900,27901,27902,61194,61375</link.rule.ids></links><search><creatorcontrib>Roy-Chaudhury, Prabir</creatorcontrib><creatorcontrib>Jones, Michael C.</creatorcontrib><creatorcontrib>Simpson, John G.</creatorcontrib><creatorcontrib>Macleod, Alison M.</creatorcontrib><creatorcontrib>Haites, Neva E.</creatorcontrib><creatorcontrib>Power, David A.</creatorcontrib><title>An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis</title><title>Pathology</title><description>Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFRl), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.</description><subject>epidermal growth factor receptor</subject><subject>glornerulonephritis</subject><subject>immunohistochemistry</subject><subject>Kidney</subject><subject>proliferative</subject><issn>0031-3025</issn><issn>1465-3931</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNqNkM9KAzEQxoMoWKsP4C0vsJo0u9sET6X4Dwpe9LykyaSbspssSbbak69uSgUPgsgcZpiZ72Pmh9A1JTeMEnFLCKOMzAQjIgev6Ama0LKuCiYYPUWTw7zIC9U5uohxSwgpOecT9Llw2Pb96HxrY_Kd31glOxzTqPfYGwyD1RD63NoE_55abKRKPuAACoZDIZ3GDsafBnwMAWK0Phs7PATfWQNBJrsDvOl8D2HsvIOhDTbZeInOjOwiXH3nKXp7uH9dPhWrl8fn5WJVqLKcpUJKCZzXQszWWsw4cFORUq2JWXMtaj43QkOt1qwiUjBDCRG01mJeU8YM04SzKaJHXxV8jAFMMwTby7BvKGkOBJtfBLPm7qixzvjMoAXZpVbJAM3Wj8Hle_-jhvzWzkJoorLgFGibWaVGe_uH-guZyIyH</recordid><startdate>1993</startdate><enddate>1993</enddate><creator>Roy-Chaudhury, Prabir</creator><creator>Jones, Michael C.</creator><creator>Simpson, John G.</creator><creator>Macleod, Alison M.</creator><creator>Haites, Neva E.</creator><creator>Power, David A.</creator><general>Elsevier B.V</general><general>Informa UK Ltd</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>1993</creationdate><title>An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis</title><author>Roy-Chaudhury, Prabir ; Jones, Michael C. ; Simpson, John G. ; Macleod, Alison M. ; Haites, Neva E. ; Power, David A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-aaae886992bd928e8f504cb0fb8d9687f9de6cb350a93f100916d976133f3d083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>epidermal growth factor receptor</topic><topic>glornerulonephritis</topic><topic>immunohistochemistry</topic><topic>Kidney</topic><topic>proliferative</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roy-Chaudhury, Prabir</creatorcontrib><creatorcontrib>Jones, Michael C.</creatorcontrib><creatorcontrib>Simpson, John G.</creatorcontrib><creatorcontrib>Macleod, Alison M.</creatorcontrib><creatorcontrib>Haites, Neva E.</creatorcontrib><creatorcontrib>Power, David A.</creatorcontrib><collection>CrossRef</collection><jtitle>Pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roy-Chaudhury, Prabir</au><au>Jones, Michael C.</au><au>Simpson, John G.</au><au>Macleod, Alison M.</au><au>Haites, Neva E.</au><au>Power, David A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis</atitle><jtitle>Pathology</jtitle><date>1993</date><risdate>1993</risdate><volume>25</volume><issue>4</issue><spage>327</spage><epage>332</epage><pages>327-332</pages><issn>0031-3025</issn><eissn>1465-3931</eissn><abstract>Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFRl), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.</abstract><pub>Elsevier B.V</pub><doi>10.3109/00313029309090851</doi><tpages>6</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0031-3025
ispartof Pathology, 1993, Vol.25 (4), p.327-332
issn 0031-3025
1465-3931
language eng
recordid cdi_crossref_primary_10_3109_00313029309090851
source Taylor & Francis; Alma/SFX Local Collection
subjects epidermal growth factor receptor
glornerulonephritis
immunohistochemistry
Kidney
proliferative
title An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T04%3A58%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-elsevier_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=An%20immunohistological%20study%20of%20epidermal%20growth%20factor%20receptor%20and%20neu%20receptor%20expression%20in%20proliferative%20glomerulonephritis&rft.jtitle=Pathology&rft.au=Roy-Chaudhury,%20Prabir&rft.date=1993&rft.volume=25&rft.issue=4&rft.spage=327&rft.epage=332&rft.pages=327-332&rft.issn=0031-3025&rft.eissn=1465-3931&rft_id=info:doi/10.3109/00313029309090851&rft_dat=%3Celsevier_cross%3ES0031302516355684%3C/elsevier_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/&rft_els_id=S0031302516355684&rfr_iscdi=true