<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wagner MC</submitter><funding>NIDDK NIH HHS</funding><pagination>35579-89</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2602882</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>283(51)</volume><pubmed_abstract>Glomerular injury is often characterized by the effacement of podocytes, loss of slit diaphragms, and proteinuria. Renal ischemia or the loss of blood flow to the kidneys has been widely associated with tubular and endothelial injury but rarely has been shown to induce podocyte damage and disruption of the slit diaphragm. In this study, we have used an in vivo rat ischemic model to demonstrate that renal ischemia induces podocyte effacement with loss of slit diaphragm and proteinuria. Biochemical analysis of the ischemic glomerulus shows that ischemia induces rapid loss of interaction between slit diaphragm junctional proteins Neph1 and ZO-1. To further understand the effect of ischemia on molecular interactions between slit diaphragm proteins, a cell culture model was employed to study th</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Ischemic injury to kidney induces glomerular podocyte effacement and dissociation of slit diaphragm proteins Neph1 and ZO-1.</pubmed_title><pmcid>PMC2602882</pmcid><funding_grant_id>K08 DK081403</funding_grant_id><funding_grant_id>K08 DK081403-01</funding_grant_id><funding_grant_id>R01 DK069408</funding_grant_id><funding_grant_id>P50 DK061594</funding_grant_id><funding_grant_id>K01 DK072047-03</funding_grant_id><pubmed_authors>Rhodes G</pubmed_authors><pubmed_authors>Verma R</pubmed_authors><pubmed_authors>Gattone V</pubmed_authors><pubmed_authors>Holzman LB</pubmed_authors><pubmed_authors>Pruthi V</pubmed_authors><pubmed_authors>Wang E</pubmed_authors><pubmed_authors>Garg P</pubmed_authors><pubmed_authors>Arif E</pubmed_authors><pubmed_authors>Wagner MC</pubmed_authors><pubmed_authors>Wean SE</pubmed_authors><pubmed_authors>Nihalani D</pubmed_authors><pubmed_authors>Saleem MA</pubmed_authors><pubmed_authors>Molitoris BA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ischemic injury to kidney induces glomerular podocyte effacement and dissociation of slit diaphragm proteins Neph1 and ZO-1.</name><description>Glomerular injury is often characterized by the effacement of podocytes, loss of slit diaphragms, and proteinuria. Renal ischemia or the loss of blood flow to the kidneys has been widely associated with tubular and endothelial injury but rarely has been shown to induce podocyte damage and disruption of the slit diaphragm. In this study, we have used an in vivo rat ischemic model to demonstrate that renal ischemia induces podocyte effacement with loss of slit diaphragm and proteinuria. Biochemical analysis of the ischemic glomerulus shows that ischemia induces rapid loss of interaction between slit diaphragm junctional proteins Neph1 and ZO-1. To further understand the effect of ischemia on molecular interactions between slit diaphragm proteins, a cell culture model was employed to study th</description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 Dec</publication><modification>2025-04-26T00:31:12.007Z</modification><creation>2019-03-27T00:19:48Z</creation></dates><accession>S-EPMC2602882</accession><cross_references><pubmed>18922801</pubmed><doi>10.1074/jbc.M805507200</doi><doi>10.1074/jbc.m805507200</doi></cross_references></HashMap>