dc.contributor.author |
Wasik AA |
|
dc.contributor.author |
Koskelainen S |
|
dc.contributor.author |
Hyvönen ME |
|
dc.contributor.author |
Musante L |
|
dc.contributor.author |
Lehtonen E |
|
dc.contributor.author |
Koskenniemi K |
|
dc.contributor.author |
Tienari J |
|
dc.contributor.author |
Vaheri A |
|
dc.contributor.author |
Kerjaschki D |
|
dc.contributor.author |
Szalay, Csaba Imre |
|
dc.contributor.author |
Révész C |
|
dc.contributor.author |
Varmanen P |
|
dc.contributor.author |
Nyman TA |
|
dc.contributor.author |
Hamar, Péter |
|
dc.contributor.author |
Holthöfer H |
|
dc.contributor.author |
Lehtonen S |
|
dc.date.accessioned |
2016-10-12T07:07:26Z |
|
dc.date.available |
2016-10-12T07:07:26Z |
|
dc.date.issued |
2014 |
|
dc.identifier |
84900992930 |
|
dc.identifier.citation |
pagination=1727-1739;
journalVolume=184;
journalIssueNumber=6;
journalTitle=AMERICAN JOURNAL OF PATHOLOGY; |
|
dc.identifier.uri |
http://repo.lib.semmelweis.hu//handle/123456789/1186 |
|
dc.identifier.uri |
doi:10.1016/j.ajpath.2014.03.002 |
|
dc.description.abstract |
Diabetic nephropathy is a complication of diabetes and a major cause of end-stage renal disease. To characterize the early pathophysiological mechanisms leading to glomerular podocyte injury in diabetic nephropathy, we performed quantitative proteomic profiling of glomeruli isolated from rats with streptozotocin-induced diabetes and controls. Fluorescence-based two-dimensional difference gel electrophoresis, coupled with mass spectrometry, identified 29 differentially expressed spots, including actin-binding protein ezrin and its interaction partner, NHERF2, which were down-regulated in the streptozotocin group. Knockdown of ezrin by siRNA in cultured podocytes increased glucose uptake compared with control siRNA-transfected cells, apparently by increasing translocation of glucose transporter GLUT1 to the plasma membrane. Knockdown of ezrin also induced actin remodeling under basal conditions, but reduced insulin-stimulated actin reorganization. Ezrin-dependent actin remodeling involved cofilin-1 that is essential for the turnover and reorganization of actin filaments. Phosphorylated, inactive cofilin-1 was up-regulated in diabetic glomeruli, suggesting altered actin dynamics. Furthermore, IHC analysis revealed reduced expression of ezrin in the podocytes of patients with diabetes. Our findings suggest that ezrin may play a role in the development of the renal complication in diabetes by regulating transport of glucose and organization of the actin cytoskeleton in podocytes. Copyright © 2014 American Society for Investigative Pathology. |
|
dc.relation.ispartof |
urn:issn:0002-9440 |
|
dc.title |
Ezrin is down-regulated in diabetic kidney glomeruli and regulates actin reorganization and glucose uptake via GLUT1 in cultured podocytes |
|
dc.type |
Journal Article |
|
dc.date.updated |
2015-01-22T14:01:36Z |
|
dc.language.rfc3066 |
en |
|
dc.identifier.mtmt |
2603895 |
|
dc.identifier.wos |
000336948700011 |
|
dc.identifier.pubmed |
24726496 |
|
dc.contributor.department |
SE/AOK/I/Kórélettani Intézet |
|
dc.contributor.institution |
Semmelweis Egyetem |
|