No complement receptor 1 stumps on podocytes in human glomerulopathies
No complement receptor 1 stumps on podocytes in human glomerulopathies. Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed b...
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| Veröffentlicht in: | Kidney international 2001-01, Vol.59 (1), p.160-168 |
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| creator | Moll, Solange Miot, Sylvie Sadallah, Salima Gudat, Fred Mihatsch, Michael J. Schifferli, Jürg A. |
| description | No complement receptor 1 stumps on podocytes in human glomerulopathies.
Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane.
To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy.
In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections.
These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack. |
| doi_str_mv | 10.1046/j.1523-1755.2001.00476.x |
| format | Article |
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Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane.
To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy.
In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections.
These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2001.00476.x</identifier><identifier>PMID: 11135068</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Antibodies, Monoclonal ; Biological and medical sciences ; CR1 stump ; Epithelial Cells - metabolism ; focal segmental glomerulosclerosis ; Glomerulonephritis ; Glomerulonephritis, IGA - metabolism ; Glomerulonephritis, IGA - pathology ; Glomerulonephritis, Membranous - metabolism ; Glomerulonephritis, Membranous - pathology ; glycoprotein ; Humans ; IgA nephritis ; Immunohistochemistry ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidney Glomerulus - metabolism ; Kidney Glomerulus - pathology ; Lupus Nephritis - metabolism ; Lupus Nephritis - pathology ; Medical sciences ; membranous nephritis ; Nephritis - metabolism ; Nephritis - pathology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Nephrosis, Lipoid - metabolism ; Nephrosis, Lipoid - pathology ; Receptors, Complement 3b - metabolism ; Reference Values ; systemic lupus erythematosus</subject><ispartof>Kidney international, 2001-01, Vol.59 (1), p.160-168</ispartof><rights>2001 International Society of Nephrology</rights><rights>2001 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-f5cc8945f7c559afa1d45ebc84133f7853c9d5f9b9b3bb3a93fef8ca44d267493</citedby><cites>FETCH-LOGICAL-c475t-f5cc8945f7c559afa1d45ebc84133f7853c9d5f9b9b3bb3a93fef8ca44d267493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210114444?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,777,781,4010,27904,27905,27906,64364,64366,64368,72218</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=919324$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11135068$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moll, Solange</creatorcontrib><creatorcontrib>Miot, Sylvie</creatorcontrib><creatorcontrib>Sadallah, Salima</creatorcontrib><creatorcontrib>Gudat, Fred</creatorcontrib><creatorcontrib>Mihatsch, Michael J.</creatorcontrib><creatorcontrib>Schifferli, Jürg A.</creatorcontrib><title>No complement receptor 1 stumps on podocytes in human glomerulopathies</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>No complement receptor 1 stumps on podocytes in human glomerulopathies.
Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane.
To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy.
In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections.
These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack.</description><subject>Antibodies, Monoclonal</subject><subject>Biological and medical sciences</subject><subject>CR1 stump</subject><subject>Epithelial Cells - metabolism</subject><subject>focal segmental glomerulosclerosis</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis, IGA - metabolism</subject><subject>Glomerulonephritis, IGA - pathology</subject><subject>Glomerulonephritis, Membranous - metabolism</subject><subject>Glomerulonephritis, Membranous - pathology</subject><subject>glycoprotein</subject><subject>Humans</subject><subject>IgA nephritis</subject><subject>Immunohistochemistry</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Glomerulus - metabolism</subject><subject>Kidney Glomerulus - pathology</subject><subject>Lupus Nephritis - metabolism</subject><subject>Lupus Nephritis - pathology</subject><subject>Medical sciences</subject><subject>membranous nephritis</subject><subject>Nephritis - metabolism</subject><subject>Nephritis - pathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Nephrosis, Lipoid - metabolism</subject><subject>Nephrosis, Lipoid - pathology</subject><subject>Receptors, Complement 3b - metabolism</subject><subject>Reference Values</subject><subject>systemic lupus erythematosus</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkcFu1DAQhi0EokvhFZAFErcEO_Zs7CNUFJCq9lLOluOMqVdJHOwEtW9fh10ViQtzsUbzzejXZ0IoZzVncv_xUHNoRMVbgLphjNeMyXZf3z8ju6fBc7JjTEHVgFBn5FXOB1Z6LdhLcsY5F8D2akcuryN1cZwHHHFaaEKH8xIT5TQv6zhnGic6xz66hwUzDRO9W0c70Z9DHDGtQ5ztchcwvyYvvB0yvjm95-TH5Zfbi2_V1c3X7xefrionW1gqD84pLcG3DkBbb3kvATunJBfCtwqE0z143elOdJ2wWnj0ylkp-2bfSi3OyYfj3TnFXyvmxYwhOxwGO2Fcs2kZgBIgC_juH_AQ1zSVbKbhjHNZqkDqCLkUc07ozZzCaNOD4cxsos3BbD7N5tNsos0f0ea-rL493V-7Efu_iyezBXh_Amx2dvDJTi7kJ05zLZotwecjhUXa74DJZBdwctiH8hWL6WP4f5ZHA9ibqQ</recordid><startdate>200101</startdate><enddate>200101</enddate><creator>Moll, Solange</creator><creator>Miot, Sylvie</creator><creator>Sadallah, Salima</creator><creator>Gudat, Fred</creator><creator>Mihatsch, Michael J.</creator><creator>Schifferli, Jürg A.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200101</creationdate><title>No complement receptor 1 stumps on podocytes in human glomerulopathies</title><author>Moll, Solange ; Miot, Sylvie ; Sadallah, Salima ; Gudat, Fred ; Mihatsch, Michael J. ; Schifferli, Jürg A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-f5cc8945f7c559afa1d45ebc84133f7853c9d5f9b9b3bb3a93fef8ca44d267493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Antibodies, Monoclonal</topic><topic>Biological and medical sciences</topic><topic>CR1 stump</topic><topic>Epithelial Cells - metabolism</topic><topic>focal segmental glomerulosclerosis</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis, IGA - metabolism</topic><topic>Glomerulonephritis, IGA - pathology</topic><topic>Glomerulonephritis, Membranous - metabolism</topic><topic>Glomerulonephritis, Membranous - pathology</topic><topic>glycoprotein</topic><topic>Humans</topic><topic>IgA nephritis</topic><topic>Immunohistochemistry</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Glomerulus - metabolism</topic><topic>Kidney Glomerulus - pathology</topic><topic>Lupus Nephritis - metabolism</topic><topic>Lupus Nephritis - pathology</topic><topic>Medical sciences</topic><topic>membranous nephritis</topic><topic>Nephritis - metabolism</topic><topic>Nephritis - pathology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Nephrosis, Lipoid - metabolism</topic><topic>Nephrosis, Lipoid - pathology</topic><topic>Receptors, Complement 3b - metabolism</topic><topic>Reference Values</topic><topic>systemic lupus erythematosus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moll, Solange</creatorcontrib><creatorcontrib>Miot, Sylvie</creatorcontrib><creatorcontrib>Sadallah, Salima</creatorcontrib><creatorcontrib>Gudat, Fred</creatorcontrib><creatorcontrib>Mihatsch, Michael J.</creatorcontrib><creatorcontrib>Schifferli, Jürg A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moll, Solange</au><au>Miot, Sylvie</au><au>Sadallah, Salima</au><au>Gudat, Fred</au><au>Mihatsch, Michael J.</au><au>Schifferli, Jürg A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>No complement receptor 1 stumps on podocytes in human glomerulopathies</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2001-01</date><risdate>2001</risdate><volume>59</volume><issue>1</issue><spage>160</spage><epage>168</epage><pages>160-168</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>No complement receptor 1 stumps on podocytes in human glomerulopathies.
Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane.
To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy.
In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections.
These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11135068</pmid><doi>10.1046/j.1523-1755.2001.00476.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies, Monoclonal Biological and medical sciences CR1 stump Epithelial Cells - metabolism focal segmental glomerulosclerosis Glomerulonephritis Glomerulonephritis, IGA - metabolism Glomerulonephritis, IGA - pathology Glomerulonephritis, Membranous - metabolism Glomerulonephritis, Membranous - pathology glycoprotein Humans IgA nephritis Immunohistochemistry Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Glomerulus - metabolism Kidney Glomerulus - pathology Lupus Nephritis - metabolism Lupus Nephritis - pathology Medical sciences membranous nephritis Nephritis - metabolism Nephritis - pathology Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Nephrosis, Lipoid - metabolism Nephrosis, Lipoid - pathology Receptors, Complement 3b - metabolism Reference Values systemic lupus erythematosus |
| title | No complement receptor 1 stumps on podocytes in human glomerulopathies |
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