Novel growth factors involved in the pathogenesis of proliferative vitreoretinopathy
To determine whether hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) are expressed in human specimens of proliferative vitreoretinopathy (PVR) and to propose a model of PVR pathogenesis based upon the known activities of these growth factors. Methods Immunohistochemical met...
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| Veröffentlicht in: | Eye (London) 2002-07, Vol.16 (4), p.422-428 |
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| description | To determine whether hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) are expressed in human specimens of proliferative vitreoretinopathy (PVR) and to propose a model of PVR pathogenesis based upon the known activities of these growth factors. Methods Immunohistochemical methods (ABC Elite) were used to demonstrate the presence of HGF and CTGF in cryostat sections of five human PVR membranes.
In each of the five PVR membranes, stromal cells were immunohistochemically positive for both HGF and CTGF. Based upon this information and the known actions of these growth factors, a model of PVR pathogenesis was developed. In this model, injury of the retina induces an inflammatory response that upregulates HGF expression inducing the formation of multilayered groups of migratory retinal pigment epithelial cells (RPE). These RPE, present in a provisional extracellular matrix, come in contact with vitreous containing TGF-beta. The TGF-beta is activated, upregulating expression of CTGF. Under the influence of TGF-beta and CTGF, RPE become myofibroblastic and fibrosis ensues. Retinal traction induces further detachment continuing the cycle of retinal injury.
HGF and CTGF are expressed in PVR membranes and may play important roles in the pathogenesis of PVR. The expression and function of these growth factors should be critically examined in human PVR specimens, in in vitro cultures of RPE, and in animal models of PVR. |
| doi_str_mv | 10.1038/sj.eye.6700190 |
| format | Article |
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In each of the five PVR membranes, stromal cells were immunohistochemically positive for both HGF and CTGF. Based upon this information and the known actions of these growth factors, a model of PVR pathogenesis was developed. In this model, injury of the retina induces an inflammatory response that upregulates HGF expression inducing the formation of multilayered groups of migratory retinal pigment epithelial cells (RPE). These RPE, present in a provisional extracellular matrix, come in contact with vitreous containing TGF-beta. The TGF-beta is activated, upregulating expression of CTGF. Under the influence of TGF-beta and CTGF, RPE become myofibroblastic and fibrosis ensues. Retinal traction induces further detachment continuing the cycle of retinal injury.
HGF and CTGF are expressed in PVR membranes and may play important roles in the pathogenesis of PVR. The expression and function of these growth factors should be critically examined in human PVR specimens, in in vitro cultures of RPE, and in animal models of PVR.</description><identifier>ISSN: 0950-222X</identifier><identifier>EISSN: 1476-5454</identifier><identifier>DOI: 10.1038/sj.eye.6700190</identifier><identifier>PMID: 12101449</identifier><identifier>CODEN: EYEEEC</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing Group</publisher><subject>Biological and medical sciences ; Connective Tissue Growth Factor ; Growth Substances - metabolism ; Hepatocyte Growth Factor - metabolism ; Humans ; Immediate-Early Proteins - metabolism ; Immunoenzyme Techniques ; Intercellular Signaling Peptides and Proteins ; Medical sciences ; Models, Biological ; Ophthalmology ; Retinopathies ; Stromal Cells - metabolism ; Transforming Growth Factor beta - metabolism ; Up-Regulation ; Vitreoretinopathy, Proliferative - etiology ; Vitreoretinopathy, Proliferative - metabolism</subject><ispartof>Eye (London), 2002-07, Vol.16 (4), p.422-428</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-9bed0057527ef284bf165d465e9c423988e384238bcb48893e4429723da806033</citedby><cites>FETCH-LOGICAL-c476t-9bed0057527ef284bf165d465e9c423988e384238bcb48893e4429723da806033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>310,311,315,782,786,791,792,23939,23940,25149,27933,27934</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13793478$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12101449$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HINTON, D. R</creatorcontrib><creatorcontrib>HE, S</creatorcontrib><creatorcontrib>JIN, M. L</creatorcontrib><creatorcontrib>BARRON, E</creatorcontrib><creatorcontrib>RYAN, S. J</creatorcontrib><title>Novel growth factors involved in the pathogenesis of proliferative vitreoretinopathy</title><title>Eye (London)</title><addtitle>Eye (Lond)</addtitle><description>To determine whether hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) are expressed in human specimens of proliferative vitreoretinopathy (PVR) and to propose a model of PVR pathogenesis based upon the known activities of these growth factors. Methods Immunohistochemical methods (ABC Elite) were used to demonstrate the presence of HGF and CTGF in cryostat sections of five human PVR membranes.
In each of the five PVR membranes, stromal cells were immunohistochemically positive for both HGF and CTGF. Based upon this information and the known actions of these growth factors, a model of PVR pathogenesis was developed. In this model, injury of the retina induces an inflammatory response that upregulates HGF expression inducing the formation of multilayered groups of migratory retinal pigment epithelial cells (RPE). These RPE, present in a provisional extracellular matrix, come in contact with vitreous containing TGF-beta. The TGF-beta is activated, upregulating expression of CTGF. Under the influence of TGF-beta and CTGF, RPE become myofibroblastic and fibrosis ensues. Retinal traction induces further detachment continuing the cycle of retinal injury.
HGF and CTGF are expressed in PVR membranes and may play important roles in the pathogenesis of PVR. The expression and function of these growth factors should be critically examined in human PVR specimens, in in vitro cultures of RPE, and in animal models of PVR.</description><subject>Biological and medical sciences</subject><subject>Connective Tissue Growth Factor</subject><subject>Growth Substances - metabolism</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>Humans</subject><subject>Immediate-Early Proteins - metabolism</subject><subject>Immunoenzyme Techniques</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Ophthalmology</subject><subject>Retinopathies</subject><subject>Stromal Cells - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Up-Regulation</subject><subject>Vitreoretinopathy, Proliferative - etiology</subject><subject>Vitreoretinopathy, Proliferative - metabolism</subject><issn>0950-222X</issn><issn>1476-5454</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpd0M1r2zAYBnAxVtY027W3DVNob071ZUs6jtAvCO0lhd2EbL9uFBwrk2SP_PdViddCT3oOP73vy4PQOcELgpm8DtsFHGBRCoyJwl_QjHBR5gUv-Fc0w6rAOaX0zyk6C2GbCBcCf0OnhJKUuZqh9aMboctevPsXN1lr6uh8yGw_um6EJoUsbiDbm7hxL9BDsCFzbbb3rrMteBPtCNloowfnIdrevcnDd3TSmi7Aj-mdo-fbm_XyPl893T0sf6_yOh0Zc1VBg3EhCiqgpZJXLSmLhpcFqJpTpqQEJlOQVV1xKRUDzqkSlDVG4hIzNkdXx7npnr8DhKh3NtTQdaYHNwQtiJRlqibBi09w6wbfp9s0JZJJgYVKaHFEtXcheGj13tud8QdNsH4rW4etTmXrqez04dc0dah20Hzwqd0ELidgQm261pu-tuHDsbSVC5ncz6PrTRw8vIP_i14BmT6R5w</recordid><startdate>20020701</startdate><enddate>20020701</enddate><creator>HINTON, D. 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R ; HE, S ; JIN, M. L ; BARRON, E ; RYAN, S. J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-9bed0057527ef284bf165d465e9c423988e384238bcb48893e4429723da806033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Biological and medical sciences</topic><topic>Connective Tissue Growth Factor</topic><topic>Growth Substances - metabolism</topic><topic>Hepatocyte Growth Factor - metabolism</topic><topic>Humans</topic><topic>Immediate-Early Proteins - metabolism</topic><topic>Immunoenzyme Techniques</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Ophthalmology</topic><topic>Retinopathies</topic><topic>Stromal Cells - metabolism</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Up-Regulation</topic><topic>Vitreoretinopathy, Proliferative - etiology</topic><topic>Vitreoretinopathy, Proliferative - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HINTON, D. 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R</au><au>HE, S</au><au>JIN, M. L</au><au>BARRON, E</au><au>RYAN, S. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel growth factors involved in the pathogenesis of proliferative vitreoretinopathy</atitle><jtitle>Eye (London)</jtitle><addtitle>Eye (Lond)</addtitle><date>2002-07-01</date><risdate>2002</risdate><volume>16</volume><issue>4</issue><spage>422</spage><epage>428</epage><pages>422-428</pages><issn>0950-222X</issn><eissn>1476-5454</eissn><coden>EYEEEC</coden><abstract>To determine whether hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) are expressed in human specimens of proliferative vitreoretinopathy (PVR) and to propose a model of PVR pathogenesis based upon the known activities of these growth factors. Methods Immunohistochemical methods (ABC Elite) were used to demonstrate the presence of HGF and CTGF in cryostat sections of five human PVR membranes.
In each of the five PVR membranes, stromal cells were immunohistochemically positive for both HGF and CTGF. Based upon this information and the known actions of these growth factors, a model of PVR pathogenesis was developed. In this model, injury of the retina induces an inflammatory response that upregulates HGF expression inducing the formation of multilayered groups of migratory retinal pigment epithelial cells (RPE). These RPE, present in a provisional extracellular matrix, come in contact with vitreous containing TGF-beta. The TGF-beta is activated, upregulating expression of CTGF. Under the influence of TGF-beta and CTGF, RPE become myofibroblastic and fibrosis ensues. Retinal traction induces further detachment continuing the cycle of retinal injury.
HGF and CTGF are expressed in PVR membranes and may play important roles in the pathogenesis of PVR. The expression and function of these growth factors should be critically examined in human PVR specimens, in in vitro cultures of RPE, and in animal models of PVR.</abstract><cop>Basingstoke</cop><pub>Nature Publishing Group</pub><pmid>12101449</pmid><doi>10.1038/sj.eye.6700190</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Connective Tissue Growth Factor Growth Substances - metabolism Hepatocyte Growth Factor - metabolism Humans Immediate-Early Proteins - metabolism Immunoenzyme Techniques Intercellular Signaling Peptides and Proteins Medical sciences Models, Biological Ophthalmology Retinopathies Stromal Cells - metabolism Transforming Growth Factor beta - metabolism Up-Regulation Vitreoretinopathy, Proliferative - etiology Vitreoretinopathy, Proliferative - metabolism |
| title | Novel growth factors involved in the pathogenesis of proliferative vitreoretinopathy |
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