Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2
Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial ro...
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| Veröffentlicht in: | Folia histochemica et cytobiologica 2011-01, Vol.49 (3), p.472-478 |
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| creator | Ostalska-Nowicka, Danuta Malinska, Agnieszka Zabel, Maciej Witkiewicz, Wojciech Nowicki, Michal |
| description | Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p 〈 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis. |
| doi_str_mv | 10.5603/FHC.2011.0067 |
| format | Article |
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Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p 〈 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis.</description><identifier>ISSN: 0239-8508</identifier><identifier>EISSN: 1897-5631</identifier><identifier>DOI: 10.5603/FHC.2011.0067</identifier><identifier>PMID: 22038228</identifier><language>eng</language><publisher>Poland: Wydawnictwo Via Medica</publisher><subject>Adolescent ; Antibodies ; Child ; Child, Preschool ; Children ; Cytoplasm ; Disease Progression ; Down-Regulation ; Electron microscopy ; Female ; Growth factors ; Humans ; Immunohistochemistry ; Inflammation ; Kidney diseases ; Male ; Monoclonal antibodies ; Nephrotic syndrome ; Nephrotic Syndrome - pathology ; Nephrotic Syndrome - physiopathology ; Overexpression ; Podocytes - metabolism ; Podocytes - ultrastructure ; Protein Isoforms - metabolism ; Receptors ; Signal Transduction - physiology ; Steroid hormones ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor C - metabolism ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Vascular endothelial growth factor receptors</subject><ispartof>Folia histochemica et cytobiologica, 2011-01, Vol.49 (3), p.472-478</ispartof><rights>Copyright Folia Histochemica et Cytobiologica 2011</rights><rights>2011. 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VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis.</description><subject>Adolescent</subject><subject>Antibodies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Children</subject><subject>Cytoplasm</subject><subject>Disease Progression</subject><subject>Down-Regulation</subject><subject>Electron microscopy</subject><subject>Female</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Male</subject><subject>Monoclonal antibodies</subject><subject>Nephrotic syndrome</subject><subject>Nephrotic Syndrome - pathology</subject><subject>Nephrotic Syndrome - physiopathology</subject><subject>Overexpression</subject><subject>Podocytes - metabolism</subject><subject>Podocytes - ultrastructure</subject><subject>Protein Isoforms - metabolism</subject><subject>Receptors</subject><subject>Signal Transduction - physiology</subject><subject>Steroid hormones</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor C - metabolism</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Vascular endothelial growth factor receptors</subject><issn>0239-8508</issn><issn>1897-5631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtr3DAQgEVoabZJj7kWQQ9pD96MNLYlH8OSTQohgZD2amR5nHXwWq5kZ9k_0N8dmTwOPfQ0w_DNg_kYOxGwzHLAs_XVailBiCVArg7YQuhCJVmO4gNbgMQi0RnoQ_Y5hEeA2JGKT-xQSkAtpV6wvzc0bLwbW8vDvq-92xKf-sY8OW-qjrh1kw9z8J46M1Lgu3bc8Nrtek8PUyy1rueu4YOrnd2PxJ9MsLHuOfW1GzfUtabjD97tYltj7Og892RpmJPvvy8u13c_EnnMPjamC_TlNR6xX-uL-9VVcn17-XN1fp1YTPWYNLKiRiNoWxkQlUpFmiq0MmYqRYWVUdAQUWURq0IplRWZVqbWcWGdo8Ejdvoyd_Duz0RhLLdtsNR1pic3hbIAgZCjxkh--4d8jK_o43GlzAupIRc6-x8lQMQn51FFpJIXynoXgqemHHy7NX4foXK2WEaL5WyxnC1G_uvr1KnaUv1Ov2nDZ8FTmMs</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Ostalska-Nowicka, Danuta</creator><creator>Malinska, Agnieszka</creator><creator>Zabel, Maciej</creator><creator>Witkiewicz, Wojciech</creator><creator>Nowicki, Michal</creator><general>Wydawnictwo Via Medica</general><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>4T-</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BYOGL</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20110101</creationdate><title>Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2</title><author>Ostalska-Nowicka, Danuta ; Malinska, Agnieszka ; Zabel, Maciej ; Witkiewicz, Wojciech ; Nowicki, Michal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-f2bef8308cba01b7414473c2b7474373ba70feeebc33b977759587ad8eced63a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adolescent</topic><topic>Antibodies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Children</topic><topic>Cytoplasm</topic><topic>Disease Progression</topic><topic>Down-Regulation</topic><topic>Electron microscopy</topic><topic>Female</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Kidney diseases</topic><topic>Male</topic><topic>Monoclonal antibodies</topic><topic>Nephrotic syndrome</topic><topic>Nephrotic Syndrome - 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Academic</collection><jtitle>Folia histochemica et cytobiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ostalska-Nowicka, Danuta</au><au>Malinska, Agnieszka</au><au>Zabel, Maciej</au><au>Witkiewicz, Wojciech</au><au>Nowicki, Michal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2</atitle><jtitle>Folia histochemica et cytobiologica</jtitle><addtitle>Folia Histochem Cytobiol</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>49</volume><issue>3</issue><spage>472</spage><epage>478</epage><pages>472-478</pages><issn>0239-8508</issn><eissn>1897-5631</eissn><abstract>Idiopathic nephrotic syndrome (INS) in children is most commonly caused by primary glomerulopathies. Morphological lesions observed in INS might be secondary to inflammatory factors of mainly extra-renal origin. The vascular endothelial growth factor (VEGF) family is regarded as playing a crucial role in this pathomechanism. The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. The study group comprised 18 children with minimal change disease (MCD), 30 patients diagnosed with diffuse mesangial proliferation (DMP) and 11 subjects with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical assay employing monoclonal anti-VEGF-C and anti-VEGFR-2 antibodies was applied in the study. The immunohistochemical expression of VEGF-C within podocyte cytoplasm was significantly increased in DMP subjects who were resistant to steroids and in all FSGS patients compared to MCD children and controls (p 〈 0.05). VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. Nephrotic syndrome progression correlates with the downregulation of podocyte VEGFR-2. For this reason, decreased VEGFR-2 expression in the podocyte processes of children with idiopathic nephrotic syndrome might be regarded as a potent factor of unfavorable prognosis.</abstract><cop>Poland</cop><pub>Wydawnictwo Via Medica</pub><pmid>22038228</pmid><doi>10.5603/FHC.2011.0067</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Antibodies Child Child, Preschool Children Cytoplasm Disease Progression Down-Regulation Electron microscopy Female Growth factors Humans Immunohistochemistry Inflammation Kidney diseases Male Monoclonal antibodies Nephrotic syndrome Nephrotic Syndrome - pathology Nephrotic Syndrome - physiopathology Overexpression Podocytes - metabolism Podocytes - ultrastructure Protein Isoforms - metabolism Receptors Signal Transduction - physiology Steroid hormones Vascular endothelial growth factor Vascular Endothelial Growth Factor C - metabolism Vascular Endothelial Growth Factor Receptor-2 - metabolism Vascular endothelial growth factor receptors |
| title | Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGFR)-2 |
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