File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Direct effects of dexamethasone on human podocytes

TitleDirect effects of dexamethasone on human podocytes
Authors
Issue Date2006
Citation
Kidney International, 2006, v. 70 n. 6, p. 1038-1045 How to Cite?
AbstractGlucocorticoids are widely used in the treatment of human glomerular diseases, but their mode of action is poorly understood particularly in steroid-sensitive nephrotic syndrome, which is most common in childhood and is characterized by a lack of inflammation in the kidney. The podocyte is a key cell in the glomerulus in health and disease: until recently, human podocytes have been difficult to study in vitro. We have developed a conditionally immortalized human podocyte cell line transfected with a temperature-sensitive simian virus 40 transgene: when the transgene is inactivated in vitro, these cells adopt the phenotype of differentiated podocytes. We have used these cells to evaluate, using immunocytochemistry, reverse transcriptase-polymerase chain reaction, and Western blotting, direct effects of the glucocorticoid dexamethasone at concentrations designed to mimic in vivo therapeutic corticosteroid levels. Dexamethasone upregulated expression of nephrin and tubulin-α, and downregulated vascular endothelial growth factor. Effects on cell cycle were complex with downregulation of cyclin kinase inhibitor p21 and augmentation of podocyte survival, without any effect on apoptosis. We report cytokine production by human podocytes, especially interleukin (IL)-6 and -8; IL-6 expression was suppressed by dexamethasone. These potent direct effects on podocytes illustrate a novel mode of action of glucocorticoids and suggest potential new therapeutic strategies for glomerular disease. © 2006 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/195439
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXing, C-Y-
dc.contributor.authorSaleem, MA-
dc.contributor.authorCoward, RJ-
dc.contributor.authorNi, L-
dc.contributor.authorWitherden, IR-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:09Z-
dc.date.available2014-02-28T06:12:09Z-
dc.date.issued2006-
dc.identifier.citationKidney International, 2006, v. 70 n. 6, p. 1038-1045-
dc.identifier.issn0085-2538-
dc.identifier.urihttp://hdl.handle.net/10722/195439-
dc.description.abstractGlucocorticoids are widely used in the treatment of human glomerular diseases, but their mode of action is poorly understood particularly in steroid-sensitive nephrotic syndrome, which is most common in childhood and is characterized by a lack of inflammation in the kidney. The podocyte is a key cell in the glomerulus in health and disease: until recently, human podocytes have been difficult to study in vitro. We have developed a conditionally immortalized human podocyte cell line transfected with a temperature-sensitive simian virus 40 transgene: when the transgene is inactivated in vitro, these cells adopt the phenotype of differentiated podocytes. We have used these cells to evaluate, using immunocytochemistry, reverse transcriptase-polymerase chain reaction, and Western blotting, direct effects of the glucocorticoid dexamethasone at concentrations designed to mimic in vivo therapeutic corticosteroid levels. Dexamethasone upregulated expression of nephrin and tubulin-α, and downregulated vascular endothelial growth factor. Effects on cell cycle were complex with downregulation of cyclin kinase inhibitor p21 and augmentation of podocyte survival, without any effect on apoptosis. We report cytokine production by human podocytes, especially interleukin (IL)-6 and -8; IL-6 expression was suppressed by dexamethasone. These potent direct effects on podocytes illustrate a novel mode of action of glucocorticoids and suggest potential new therapeutic strategies for glomerular disease. © 2006 International Society of Nephrology.-
dc.languageeng-
dc.relation.ispartofKidney International-
dc.titleDirect effects of dexamethasone on human podocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.ki.5001655-
dc.identifier.pmid16837924-
dc.identifier.scopuseid_2-s2.0-33748430642-
dc.identifier.volume70-
dc.identifier.issue6-
dc.identifier.spage1038-
dc.identifier.epage1045-
dc.identifier.isiWOS:000240370300017-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats