File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hemopexin induces nephrin-dependent reorganization of the actin cytoskeleton in podocytes

TitleHemopexin induces nephrin-dependent reorganization of the actin cytoskeleton in podocytes
Authors
Issue Date2008
Citation
Journal of the American Society of Nephrology, 2008, v. 19 n. 11, p. 2140-2149 How to Cite?
AbstractHemopexin is an abundant plasma protein that effectively scavenges heme. When infused into rats, hemopexin induces reversible proteinuria, and activated hemopexin is increased in children with minimal change nephrotic syndrome. These observations suggest a role for hemopexin in glomerular disease; in this study, the effects of active hemopexin on human podocytes and glomerular endothelial cells, the two cell types that compose the glomerular filtration barrier, were investigated. Within 30 min of treatment with hemopexin, actin reorganized from stress fibers to cytoplasmic aggregates and membrane ruffles in wild-type podocytes. This did not occur in nephrin-deficient podocytes unless they were transfected with nephrin-expressing plasmids. Furthermore, hemopexin did not affect actin organization in cells that do not express nephrin, specifically human glomerular endothelial cells, fibroblasts, and HEK293 cells. The effects of hemopexin on wild-type podocytes reversed within 4 h and were inhibited by preincubation with human plasma. Treatment with hemopexin activated protein kinase B in both wild-type and nephrin-deficient podocytes but activated RhoA only in wild-type cells. In addition, hemopexin led to a selective increase in the passage of albumin across monolayers of glomerular endothelial cells and to a reduction in glycocalyx. In summary, active hemopexin causes nephrin-dependent remodeling of podocytes and affects permeability of the glomerular filtration barrier by degrading the glycocalyx. Copyright © 2008 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/195466
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLennon, R-
dc.contributor.authorSingh, A-
dc.contributor.authorWelsh, GI-
dc.contributor.authorCoward, RJ-
dc.contributor.authorSatchell, S-
dc.contributor.authorNi, L-
dc.contributor.authorMathieson, PW-
dc.contributor.authorBakker, WW-
dc.contributor.authorSaleem, MA-
dc.date.accessioned2014-02-28T06:12:12Z-
dc.date.available2014-02-28T06:12:12Z-
dc.date.issued2008-
dc.identifier.citationJournal of the American Society of Nephrology, 2008, v. 19 n. 11, p. 2140-2149-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/195466-
dc.description.abstractHemopexin is an abundant plasma protein that effectively scavenges heme. When infused into rats, hemopexin induces reversible proteinuria, and activated hemopexin is increased in children with minimal change nephrotic syndrome. These observations suggest a role for hemopexin in glomerular disease; in this study, the effects of active hemopexin on human podocytes and glomerular endothelial cells, the two cell types that compose the glomerular filtration barrier, were investigated. Within 30 min of treatment with hemopexin, actin reorganized from stress fibers to cytoplasmic aggregates and membrane ruffles in wild-type podocytes. This did not occur in nephrin-deficient podocytes unless they were transfected with nephrin-expressing plasmids. Furthermore, hemopexin did not affect actin organization in cells that do not express nephrin, specifically human glomerular endothelial cells, fibroblasts, and HEK293 cells. The effects of hemopexin on wild-type podocytes reversed within 4 h and were inhibited by preincubation with human plasma. Treatment with hemopexin activated protein kinase B in both wild-type and nephrin-deficient podocytes but activated RhoA only in wild-type cells. In addition, hemopexin led to a selective increase in the passage of albumin across monolayers of glomerular endothelial cells and to a reduction in glycocalyx. In summary, active hemopexin causes nephrin-dependent remodeling of podocytes and affects permeability of the glomerular filtration barrier by degrading the glycocalyx. Copyright © 2008 by the American Society of Nephrology.-
dc.languageeng-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleHemopexin induces nephrin-dependent reorganization of the actin cytoskeleton in podocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1681/ASN.2007080940-
dc.identifier.pmid18753258-
dc.identifier.scopuseid_2-s2.0-55749104895-
dc.identifier.volume19-
dc.identifier.issue11-
dc.identifier.spage2140-
dc.identifier.epage2149-
dc.identifier.isiWOS:000260588100015-
dc.identifier.f10001129821-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats