Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy
Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy. Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fib...
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| Veröffentlicht in: | Kidney international 2000-01, Vol.57 (1), p.147-158 |
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| creator | Mezzano, Sergio A. Droguett, M. Alejandra Burgos, M. Eugenia Ardiles, Leopoldo G. Aros, Claudio A. Caorsi, Italo Egido, Jesús |
| description | Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy.
Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function.
Paraffin-embedded biopsy specimens from 25 patients with IMN (13 progressive and 12 nonprogressive) were retrospectively studied by immunohistochemistry [monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted chemokine (RANTES), osteopontin (OPN), platelet-derived growth factor-BB (PD-GF-BB)] and in situ hybridization [MCP-1, RANTES, PDGF-BB, transforming growth factor-β1 (TGF-β1)]. Moreover, we studied the presence of myofibroblasts, which were identified by the expression of α-smooth muscle actin (α-SMA), the monocytes/macrophages (CD68-positive cells), and T-cell infiltration (CD4+ and CD8+ cells). All of the patients were nephrotic and without treatment at time of the biopsy.
A strong up-regulation of MCP-1, RANTES, and OPN expression was observed, mainly in tubular epithelial cells, with a significant major intensity in the progressive IMN patients. A strong correlation between the mRNA expression and the corresponding protein was noted. The presence of these chemokines and OPN was associated with interstitial cell infiltration. TGF-β and PDGF were also up-regulated, mainly in tubular epithelial cells, with a stronger expression in the progressive IMN, and an association with the presence of myofibroblasts was found.
Patients with severe proteinuria and progressive IMN have an overexpression in tubular epithelial cells of the chemokines MCP-1, RANTES, and OPN and the profibrogenic cytokines PDGF-BB and TGF-β. Because this up-regulation was associated with an interstitial accumulation of mononuclear cells and an increase in myofibroblastic activity, it is suggested that those mediators are potential predictors of progression in IMN. Finally, based |
| doi_str_mv | 10.1046/j.1523-1755.2000.00830.x |
| format | Article |
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Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function.
Paraffin-embedded biopsy specimens from 25 patients with IMN (13 progressive and 12 nonprogressive) were retrospectively studied by immunohistochemistry [monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted chemokine (RANTES), osteopontin (OPN), platelet-derived growth factor-BB (PD-GF-BB)] and in situ hybridization [MCP-1, RANTES, PDGF-BB, transforming growth factor-β1 (TGF-β1)]. Moreover, we studied the presence of myofibroblasts, which were identified by the expression of α-smooth muscle actin (α-SMA), the monocytes/macrophages (CD68-positive cells), and T-cell infiltration (CD4+ and CD8+ cells). All of the patients were nephrotic and without treatment at time of the biopsy.
A strong up-regulation of MCP-1, RANTES, and OPN expression was observed, mainly in tubular epithelial cells, with a significant major intensity in the progressive IMN patients. A strong correlation between the mRNA expression and the corresponding protein was noted. The presence of these chemokines and OPN was associated with interstitial cell infiltration. TGF-β and PDGF were also up-regulated, mainly in tubular epithelial cells, with a stronger expression in the progressive IMN, and an association with the presence of myofibroblasts was found.
Patients with severe proteinuria and progressive IMN have an overexpression in tubular epithelial cells of the chemokines MCP-1, RANTES, and OPN and the profibrogenic cytokines PDGF-BB and TGF-β. Because this up-regulation was associated with an interstitial accumulation of mononuclear cells and an increase in myofibroblastic activity, it is suggested that those mediators are potential predictors of progression in IMN. Finally, based on experimental data and the findings of this article, we speculate that severe proteinuria is the main factor responsible for the up-regulation of these factors in tubular epithelial cells.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2000.00830.x</identifier><identifier>PMID: 10620196</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Chemokines - genetics ; Cytokines - genetics ; Female ; Fibroblasts - metabolism ; Glomerulonephritis, Membranous - metabolism ; Glomerulonephritis, Membranous - pathology ; growth factors ; Humans ; idiopathic membranous nephropathy ; Immunohistochemistry ; In Situ Hybridization ; Investigative techniques, diagnostic techniques (general aspects) ; Kidney - metabolism ; Macrophages - pathology ; Male ; Medical sciences ; Middle Aged ; monocyte chemoattractant protein-1 ; osteopontin ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; proteinuria ; Urinary system</subject><ispartof>Kidney international, 2000-01, Vol.57 (1), p.147-158</ispartof><rights>2000 International Society of Nephrology</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-c6bc93fd102fb3944510d44c6496bdb894e1691be9289b5a22041dd648c942313</citedby><cites>FETCH-LOGICAL-c476t-c6bc93fd102fb3944510d44c6496bdb894e1691be9289b5a22041dd648c942313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1289503$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10620196$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mezzano, Sergio A.</creatorcontrib><creatorcontrib>Droguett, M. Alejandra</creatorcontrib><creatorcontrib>Burgos, M. Eugenia</creatorcontrib><creatorcontrib>Ardiles, Leopoldo G.</creatorcontrib><creatorcontrib>Aros, Claudio A.</creatorcontrib><creatorcontrib>Caorsi, Italo</creatorcontrib><creatorcontrib>Egido, Jesús</creatorcontrib><title>Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy.
Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function.
Paraffin-embedded biopsy specimens from 25 patients with IMN (13 progressive and 12 nonprogressive) were retrospectively studied by immunohistochemistry [monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted chemokine (RANTES), osteopontin (OPN), platelet-derived growth factor-BB (PD-GF-BB)] and in situ hybridization [MCP-1, RANTES, PDGF-BB, transforming growth factor-β1 (TGF-β1)]. Moreover, we studied the presence of myofibroblasts, which were identified by the expression of α-smooth muscle actin (α-SMA), the monocytes/macrophages (CD68-positive cells), and T-cell infiltration (CD4+ and CD8+ cells). All of the patients were nephrotic and without treatment at time of the biopsy.
A strong up-regulation of MCP-1, RANTES, and OPN expression was observed, mainly in tubular epithelial cells, with a significant major intensity in the progressive IMN patients. A strong correlation between the mRNA expression and the corresponding protein was noted. The presence of these chemokines and OPN was associated with interstitial cell infiltration. TGF-β and PDGF were also up-regulated, mainly in tubular epithelial cells, with a stronger expression in the progressive IMN, and an association with the presence of myofibroblasts was found.
Patients with severe proteinuria and progressive IMN have an overexpression in tubular epithelial cells of the chemokines MCP-1, RANTES, and OPN and the profibrogenic cytokines PDGF-BB and TGF-β. Because this up-regulation was associated with an interstitial accumulation of mononuclear cells and an increase in myofibroblastic activity, it is suggested that those mediators are potential predictors of progression in IMN. Finally, based on experimental data and the findings of this article, we speculate that severe proteinuria is the main factor responsible for the up-regulation of these factors in tubular epithelial cells.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Chemokines - genetics</subject><subject>Cytokines - genetics</subject><subject>Female</subject><subject>Fibroblasts - metabolism</subject><subject>Glomerulonephritis, Membranous - metabolism</subject><subject>Glomerulonephritis, Membranous - pathology</subject><subject>growth factors</subject><subject>Humans</subject><subject>idiopathic membranous nephropathy</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Kidney - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>monocyte chemoattractant protein-1</subject><subject>osteopontin</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>proteinuria</subject><subject>Urinary system</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU2P0zAQhi0EYkvhLyALIU4kjD-SxkdY8SWttBc4W7YzoS6JXexk1f573G35EBdOlmaeGY2flxDKoGYg2ze7mjVcVGzTNDUHgBqgE1AfHpDV78ZDsirVpuKN6K7Ik5x3BeyUgMfkikHLgal2RYbbO0x42CfM2cdA40DdFqf43QfMr-ngbYrfMHhH3XH-VTWhp9Mx3jftaPKcqQ90u0wm0Aknm0yIS6YB99sU92beHp-SR4MZMz67vGvy9cP7L9efqpvbj5-v395UTm7auXKtdUoMPQM-WKGkbBj0UrpWqtb2tlMSWauYRcU7ZRvDOUjW963snJJcMLEmr8579yn-WDDPevLZ4TiagOUkvYGOAWxkAV_8A-7ikkK5TXMGDJQoqtakO0MuxZwTDnqf_GTSUTPQpyD0Tp9865NvfQpC3wehD2X0-WX_Yifs_xo8my_AywtgsjPjUJw5n_9w5YMNiIK9O2NYrN15TDo7j8Fh7xO6WffR__-Ynyb-pyY</recordid><startdate>200001</startdate><enddate>200001</enddate><creator>Mezzano, Sergio A.</creator><creator>Droguett, M. 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Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>proteinuria</topic><topic>Urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mezzano, Sergio A.</creatorcontrib><creatorcontrib>Droguett, M. Alejandra</creatorcontrib><creatorcontrib>Burgos, M. 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Alejandra</au><au>Burgos, M. Eugenia</au><au>Ardiles, Leopoldo G.</au><au>Aros, Claudio A.</au><au>Caorsi, Italo</au><au>Egido, Jesús</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2000-01</date><risdate>2000</risdate><volume>57</volume><issue>1</issue><spage>147</spage><epage>158</epage><pages>147-158</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy.
Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function.
Paraffin-embedded biopsy specimens from 25 patients with IMN (13 progressive and 12 nonprogressive) were retrospectively studied by immunohistochemistry [monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted chemokine (RANTES), osteopontin (OPN), platelet-derived growth factor-BB (PD-GF-BB)] and in situ hybridization [MCP-1, RANTES, PDGF-BB, transforming growth factor-β1 (TGF-β1)]. Moreover, we studied the presence of myofibroblasts, which were identified by the expression of α-smooth muscle actin (α-SMA), the monocytes/macrophages (CD68-positive cells), and T-cell infiltration (CD4+ and CD8+ cells). All of the patients were nephrotic and without treatment at time of the biopsy.
A strong up-regulation of MCP-1, RANTES, and OPN expression was observed, mainly in tubular epithelial cells, with a significant major intensity in the progressive IMN patients. A strong correlation between the mRNA expression and the corresponding protein was noted. The presence of these chemokines and OPN was associated with interstitial cell infiltration. TGF-β and PDGF were also up-regulated, mainly in tubular epithelial cells, with a stronger expression in the progressive IMN, and an association with the presence of myofibroblasts was found.
Patients with severe proteinuria and progressive IMN have an overexpression in tubular epithelial cells of the chemokines MCP-1, RANTES, and OPN and the profibrogenic cytokines PDGF-BB and TGF-β. Because this up-regulation was associated with an interstitial accumulation of mononuclear cells and an increase in myofibroblastic activity, it is suggested that those mediators are potential predictors of progression in IMN. Finally, based on experimental data and the findings of this article, we speculate that severe proteinuria is the main factor responsible for the up-regulation of these factors in tubular epithelial cells.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10620196</pmid><doi>10.1046/j.1523-1755.2000.00830.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Chemokines - genetics Cytokines - genetics Female Fibroblasts - metabolism Glomerulonephritis, Membranous - metabolism Glomerulonephritis, Membranous - pathology growth factors Humans idiopathic membranous nephropathy Immunohistochemistry In Situ Hybridization Investigative techniques, diagnostic techniques (general aspects) Kidney - metabolism Macrophages - pathology Male Medical sciences Middle Aged monocyte chemoattractant protein-1 osteopontin Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques proteinuria Urinary system |
| title | Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy |
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