Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells
Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells. Platelet-derived growth factor (PDGF)-B regulates mesangial cell and vessel development during embryogenesis, and contributes to the pathogenesis of adult renal and vascular diseases. Endothelial cell...
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| Veröffentlicht in: | Kidney international 2005-08, Vol.68 (2), p.695-703 |
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| creator | Eng, Eudora Holgren, Cory Hubchak, Susan Naaz, Parveen Schnaper, H. William |
| description | Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells.
Platelet-derived growth factor (PDGF)-B regulates mesangial cell and vessel development during embryogenesis, and contributes to the pathogenesis of adult renal and vascular diseases. Endothelial cell PDGF-B exerts paracrine effects on mesangial cells, but its regulation is not well defined. We examined the impact of hypoxia on PDGF-B-mediated interactions between glomerular endothelial and mesangial cells, a condition of potential relevance in developing, and diseased adult, kidneys.
Glomerular endothelial or mesangial cells were subjected to hypoxia and responses compared to normoxic cells. Endothelial PDGF-B was studied by Northern and Western analysis. Mesangial proliferative responses to PDGF-B were assessed by3H-thymidine incorporation, and migration by a modified Boyden chamber assay. Hypoxia-induced changes in receptor specific binding capacity were studied by saturation binding assays.
Hypoxia stimulated increases in endothelial PDGF-B mRNA and protein. In normoxic mesangial cells, PDGF-B stimulated dose-dependent proliferation, but the proliferative response of hypoxic cells was two to three times greater. Exogenous PDGF-B also caused prompter migration in hypoxic mesangial cells. Mesangial cells were treated with endothelial cell-conditioned medium. More cells migrated when hypoxic cells were stimulated with hypoxic conditioned medium, than when normoxic cells were stimulated with normoxic conditioned medium. Preincubating conditioned medium with PDGF-B neutralizing antibody greatly decreased the chemoattractant activity. Binding studies demonstrated increased specific binding capacity in hypoxic cells.
Hypoxia enhances PDGF-B paracrine interactions between glomerular endothelial and mesangial cells. These hypoxia-regulated interactions may be important during glomerulogenesis in fetal life and during the pathogenesis of adult glomerular disease. |
| doi_str_mv | 10.1111/j.1523-1755.2005.00448.x |
| format | Article |
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Platelet-derived growth factor (PDGF)-B regulates mesangial cell and vessel development during embryogenesis, and contributes to the pathogenesis of adult renal and vascular diseases. Endothelial cell PDGF-B exerts paracrine effects on mesangial cells, but its regulation is not well defined. We examined the impact of hypoxia on PDGF-B-mediated interactions between glomerular endothelial and mesangial cells, a condition of potential relevance in developing, and diseased adult, kidneys.
Glomerular endothelial or mesangial cells were subjected to hypoxia and responses compared to normoxic cells. Endothelial PDGF-B was studied by Northern and Western analysis. Mesangial proliferative responses to PDGF-B were assessed by3H-thymidine incorporation, and migration by a modified Boyden chamber assay. Hypoxia-induced changes in receptor specific binding capacity were studied by saturation binding assays.
Hypoxia stimulated increases in endothelial PDGF-B mRNA and protein. In normoxic mesangial cells, PDGF-B stimulated dose-dependent proliferation, but the proliferative response of hypoxic cells was two to three times greater. Exogenous PDGF-B also caused prompter migration in hypoxic mesangial cells. Mesangial cells were treated with endothelial cell-conditioned medium. More cells migrated when hypoxic cells were stimulated with hypoxic conditioned medium, than when normoxic cells were stimulated with normoxic conditioned medium. Preincubating conditioned medium with PDGF-B neutralizing antibody greatly decreased the chemoattractant activity. Binding studies demonstrated increased specific binding capacity in hypoxic cells.
Hypoxia enhances PDGF-B paracrine interactions between glomerular endothelial and mesangial cells. These hypoxia-regulated interactions may be important during glomerulogenesis in fetal life and during the pathogenesis of adult glomerular disease.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1111/j.1523-1755.2005.00448.x</identifier><identifier>PMID: 16014047</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cattle ; Cell Communication - physiology ; Cell Membrane - metabolism ; Cell Movement - physiology ; Cells, Cultured ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; glomerular endothelial cell ; Glomerular Mesangium - cytology ; Glomerular Mesangium - metabolism ; hypoxia ; Hypoxia - metabolism ; Hypoxia - pathology ; Hypoxia - physiopathology ; Hypoxia-Inducible Factor 1, alpha Subunit ; Kidney Glomerulus - blood supply ; Kidney Glomerulus - cytology ; Kidney Glomerulus - metabolism ; Medical sciences ; mesangial cell ; Nephrology. Urinary tract diseases ; PDGF-B ; PDGF-β receptor ; Protein Binding - physiology ; Proto-Oncogene Proteins c-sis - genetics ; Proto-Oncogene Proteins c-sis - metabolism ; Receptor, Platelet-Derived Growth Factor beta - metabolism ; renal organogenesis ; specific binding capacity ; Transcription Factors - metabolism ; Transcription, Genetic - physiology ; Vascular Endothelial Growth Factor A - metabolism ; vessel formation</subject><ispartof>Kidney international, 2005-08, Vol.68 (2), p.695-703</ispartof><rights>2005 International Society of Nephrology</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-6e500892feb8e32a822484e9799be5787a37b14d877c641343024a62a91ea7193</citedby><cites>FETCH-LOGICAL-c501t-6e500892feb8e32a822484e9799be5787a37b14d877c641343024a62a91ea7193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210118815?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,64366,64368,64370,72220</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17008610$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16014047$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eng, Eudora</creatorcontrib><creatorcontrib>Holgren, Cory</creatorcontrib><creatorcontrib>Hubchak, Susan</creatorcontrib><creatorcontrib>Naaz, Parveen</creatorcontrib><creatorcontrib>Schnaper, H. William</creatorcontrib><title>Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells.
Platelet-derived growth factor (PDGF)-B regulates mesangial cell and vessel development during embryogenesis, and contributes to the pathogenesis of adult renal and vascular diseases. Endothelial cell PDGF-B exerts paracrine effects on mesangial cells, but its regulation is not well defined. We examined the impact of hypoxia on PDGF-B-mediated interactions between glomerular endothelial and mesangial cells, a condition of potential relevance in developing, and diseased adult, kidneys.
Glomerular endothelial or mesangial cells were subjected to hypoxia and responses compared to normoxic cells. Endothelial PDGF-B was studied by Northern and Western analysis. Mesangial proliferative responses to PDGF-B were assessed by3H-thymidine incorporation, and migration by a modified Boyden chamber assay. Hypoxia-induced changes in receptor specific binding capacity were studied by saturation binding assays.
Hypoxia stimulated increases in endothelial PDGF-B mRNA and protein. In normoxic mesangial cells, PDGF-B stimulated dose-dependent proliferation, but the proliferative response of hypoxic cells was two to three times greater. Exogenous PDGF-B also caused prompter migration in hypoxic mesangial cells. Mesangial cells were treated with endothelial cell-conditioned medium. More cells migrated when hypoxic cells were stimulated with hypoxic conditioned medium, than when normoxic cells were stimulated with normoxic conditioned medium. Preincubating conditioned medium with PDGF-B neutralizing antibody greatly decreased the chemoattractant activity. Binding studies demonstrated increased specific binding capacity in hypoxic cells.
Hypoxia enhances PDGF-B paracrine interactions between glomerular endothelial and mesangial cells. These hypoxia-regulated interactions may be important during glomerulogenesis in fetal life and during the pathogenesis of adult glomerular disease.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cattle</subject><subject>Cell Communication - physiology</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>glomerular endothelial cell</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - metabolism</subject><subject>hypoxia</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - pathology</subject><subject>Hypoxia - physiopathology</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit</subject><subject>Kidney Glomerulus - blood supply</subject><subject>Kidney Glomerulus - cytology</subject><subject>Kidney Glomerulus - metabolism</subject><subject>Medical sciences</subject><subject>mesangial cell</subject><subject>Nephrology. Urinary tract diseases</subject><subject>PDGF-B</subject><subject>PDGF-β receptor</subject><subject>Protein Binding - physiology</subject><subject>Proto-Oncogene Proteins c-sis - genetics</subject><subject>Proto-Oncogene Proteins c-sis - metabolism</subject><subject>Receptor, Platelet-Derived Growth Factor beta - metabolism</subject><subject>renal organogenesis</subject><subject>specific binding capacity</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic - physiology</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>vessel formation</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkUFv1DAQhS0EotuFnwCykOgtwePYsXOkhbZIleAAZ8txZhevEmexk7L99zjsqpW44Is9mm9Gz-8RQoGVkM-HXQmSVwUoKUvOmCwZE0KXh2dk9dh4TlaMaVlwWekzcp7SjuW6qdhLcgY1A8GEWpH29mE_HrylEbdzbydM9Nunm-vikvowYbRu8mNItMXpN2Kg234cMGYwUmf3vs-PB4qhG6ef2HvbUxs6OmCyYbtUDvs-vSIvNrZP-Pp0r8mP68_fr26Lu683X64-3hVOMpiKGuWij2-w1VhxqzkXWmCjmqZFqbSylWpBdFopVwuoRMW4sDW3DaBV0FRrcnHcu4_jrxnTZAafFgU24DgnU2tWMah5Bt_9A-7GOYaszXBgAFqDzJA-Qi6OKUXcmH30Q_6uAWaWEMzOLF6bxWuzhGD-hmAOefTtaf_cDtg9DZ5cz8D7E2CTs_0m2uB8euJUNqIGlrk3Ry7YaY74CAjR1JAtWJPLYx-zrfceo0nOY3DY-YhuMt3o_6_2D2rFrf4</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>Eng, Eudora</creator><creator>Holgren, Cory</creator><creator>Hubchak, Susan</creator><creator>Naaz, Parveen</creator><creator>Schnaper, H. William</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>20050801</creationdate><title>Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells</title><author>Eng, Eudora ; Holgren, Cory ; Hubchak, Susan ; Naaz, Parveen ; Schnaper, H. William</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-6e500892feb8e32a822484e9799be5787a37b14d877c641343024a62a91ea7193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cattle</topic><topic>Cell Communication - physiology</topic><topic>Cell Membrane - metabolism</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>glomerular endothelial cell</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - metabolism</topic><topic>hypoxia</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - pathology</topic><topic>Hypoxia - physiopathology</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit</topic><topic>Kidney Glomerulus - blood supply</topic><topic>Kidney Glomerulus - cytology</topic><topic>Kidney Glomerulus - metabolism</topic><topic>Medical sciences</topic><topic>mesangial cell</topic><topic>Nephrology. Urinary tract diseases</topic><topic>PDGF-B</topic><topic>PDGF-β receptor</topic><topic>Protein Binding - physiology</topic><topic>Proto-Oncogene Proteins c-sis - genetics</topic><topic>Proto-Oncogene Proteins c-sis - metabolism</topic><topic>Receptor, Platelet-Derived Growth Factor beta - metabolism</topic><topic>renal organogenesis</topic><topic>specific binding capacity</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic - physiology</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>vessel formation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eng, Eudora</creatorcontrib><creatorcontrib>Holgren, Cory</creatorcontrib><creatorcontrib>Hubchak, Susan</creatorcontrib><creatorcontrib>Naaz, Parveen</creatorcontrib><creatorcontrib>Schnaper, H. 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William</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>68</volume><issue>2</issue><spage>695</spage><epage>703</epage><pages>695-703</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells.
Platelet-derived growth factor (PDGF)-B regulates mesangial cell and vessel development during embryogenesis, and contributes to the pathogenesis of adult renal and vascular diseases. Endothelial cell PDGF-B exerts paracrine effects on mesangial cells, but its regulation is not well defined. We examined the impact of hypoxia on PDGF-B-mediated interactions between glomerular endothelial and mesangial cells, a condition of potential relevance in developing, and diseased adult, kidneys.
Glomerular endothelial or mesangial cells were subjected to hypoxia and responses compared to normoxic cells. Endothelial PDGF-B was studied by Northern and Western analysis. Mesangial proliferative responses to PDGF-B were assessed by3H-thymidine incorporation, and migration by a modified Boyden chamber assay. Hypoxia-induced changes in receptor specific binding capacity were studied by saturation binding assays.
Hypoxia stimulated increases in endothelial PDGF-B mRNA and protein. In normoxic mesangial cells, PDGF-B stimulated dose-dependent proliferation, but the proliferative response of hypoxic cells was two to three times greater. Exogenous PDGF-B also caused prompter migration in hypoxic mesangial cells. Mesangial cells were treated with endothelial cell-conditioned medium. More cells migrated when hypoxic cells were stimulated with hypoxic conditioned medium, than when normoxic cells were stimulated with normoxic conditioned medium. Preincubating conditioned medium with PDGF-B neutralizing antibody greatly decreased the chemoattractant activity. Binding studies demonstrated increased specific binding capacity in hypoxic cells.
Hypoxia enhances PDGF-B paracrine interactions between glomerular endothelial and mesangial cells. These hypoxia-regulated interactions may be important during glomerulogenesis in fetal life and during the pathogenesis of adult glomerular disease.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16014047</pmid><doi>10.1111/j.1523-1755.2005.00448.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cattle Cell Communication - physiology Cell Membrane - metabolism Cell Movement - physiology Cells, Cultured Endothelial Cells - cytology Endothelial Cells - metabolism glomerular endothelial cell Glomerular Mesangium - cytology Glomerular Mesangium - metabolism hypoxia Hypoxia - metabolism Hypoxia - pathology Hypoxia - physiopathology Hypoxia-Inducible Factor 1, alpha Subunit Kidney Glomerulus - blood supply Kidney Glomerulus - cytology Kidney Glomerulus - metabolism Medical sciences mesangial cell Nephrology. Urinary tract diseases PDGF-B PDGF-β receptor Protein Binding - physiology Proto-Oncogene Proteins c-sis - genetics Proto-Oncogene Proteins c-sis - metabolism Receptor, Platelet-Derived Growth Factor beta - metabolism renal organogenesis specific binding capacity Transcription Factors - metabolism Transcription, Genetic - physiology Vascular Endothelial Growth Factor A - metabolism vessel formation |
| title | Hypoxia regulates PDGF-B interactions between glomerular capillary endothelial and mesangial cells |
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