File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Interferon-β reduces proteinuria in experimental glomerulonephritis

TitleInterferon-β reduces proteinuria in experimental glomerulonephritis
Authors
Issue Date2007
Citation
Journal of the American Society of Nephrology, 2007, v. 18 n. 11, p. 2875-2884 How to Cite?
AbstractInterferon-β (IFN-β) is a multifunctional cytokine with immunomodulatory properties. We examined the effect of IFN-β in three separate rat models of glomerular injury and in cultured human glomerular endothelial cells and podocytes. In nephrotoxic nephritis in WKY rats, recombinant rat IFN-β started either at induction or after establishment of disease significantly reduced 24-h proteinuria by up to 73% and 51%, respectively, but did not affect serum creatinine. There was a slight reduction in numbers of glomerular macrophages, but no difference in glomerular or tubulointerstitial scarring. In Thy-1 nephritis in Lewis rats, IFN-β started at induction of disease reduced proteinuria by up to 66% with no effect on numbers of glomerular macrophages, but a reduced number of proliferating cells. In puromycin nephropathy in Wistar rats, IFN-β started at induction of disease reduced proteinuria by up to 93%, but had no effect on glomerular histology. In cultured cells, human IFN-β-1a had a dramatic effect on barrier properties, increasing electrical resistance across monolayers of either glomerular endothelial cells or podocytes and decreasing trans-monolayer passage of albumin. In conclusion, these results show that IFN-β reduces proteinuria in three different rat models of glomerular injury and that its anti-proteinuric action may result from direct effects on cells that comprise the glomerular filtration barrier. These data indicate that IFN-β may have potential as a therapeutic agent in proteinuric renal disease. Copyright © 2007 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/195455
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSatchell, SC-
dc.contributor.authorBuchatska, O-
dc.contributor.authorKhan, SB-
dc.contributor.authorBhangal, G-
dc.contributor.authorTasman, CH-
dc.contributor.authorSaleem, MA-
dc.contributor.authorBaker, DP-
dc.contributor.authorLobb, RR-
dc.contributor.authorSmith, J-
dc.contributor.authorCook, HT-
dc.contributor.authorMathieson, PW-
dc.contributor.authorPusey, CD-
dc.date.accessioned2014-02-28T06:12:11Z-
dc.date.available2014-02-28T06:12:11Z-
dc.date.issued2007-
dc.identifier.citationJournal of the American Society of Nephrology, 2007, v. 18 n. 11, p. 2875-2884-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/195455-
dc.description.abstractInterferon-β (IFN-β) is a multifunctional cytokine with immunomodulatory properties. We examined the effect of IFN-β in three separate rat models of glomerular injury and in cultured human glomerular endothelial cells and podocytes. In nephrotoxic nephritis in WKY rats, recombinant rat IFN-β started either at induction or after establishment of disease significantly reduced 24-h proteinuria by up to 73% and 51%, respectively, but did not affect serum creatinine. There was a slight reduction in numbers of glomerular macrophages, but no difference in glomerular or tubulointerstitial scarring. In Thy-1 nephritis in Lewis rats, IFN-β started at induction of disease reduced proteinuria by up to 66% with no effect on numbers of glomerular macrophages, but a reduced number of proliferating cells. In puromycin nephropathy in Wistar rats, IFN-β started at induction of disease reduced proteinuria by up to 93%, but had no effect on glomerular histology. In cultured cells, human IFN-β-1a had a dramatic effect on barrier properties, increasing electrical resistance across monolayers of either glomerular endothelial cells or podocytes and decreasing trans-monolayer passage of albumin. In conclusion, these results show that IFN-β reduces proteinuria in three different rat models of glomerular injury and that its anti-proteinuric action may result from direct effects on cells that comprise the glomerular filtration barrier. These data indicate that IFN-β may have potential as a therapeutic agent in proteinuric renal disease. Copyright © 2007 by the American Society of Nephrology.-
dc.languageeng-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleInterferon-β reduces proteinuria in experimental glomerulonephritis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1681/ASN.2006101104-
dc.identifier.pmid17942968-
dc.identifier.scopuseid_2-s2.0-35848935010-
dc.identifier.volume18-
dc.identifier.issue11-
dc.identifier.spage2875-
dc.identifier.epage2884-
dc.identifier.isiWOS:000250737600015-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats