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...
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Veröffentlicht in: | Pathology 1993, Vol.25 (4), p.327-332 |
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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 |
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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> |
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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 |
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