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Article: Insulin directly stimulates VEGF-A production in the glomerular podocyte

TitleInsulin directly stimulates VEGF-A production in the glomerular podocyte
Authors
Issue Date2013
Citation
American Journal of Physiology - Renal Physiology, 2013, v. 305 n. 2, p. F182-F188 How to Cite?
AbstractPodocytes are critically important for maintaining the integrity of the glomerular filtration barrier and preventing albuminuria. Recently, it has become clear that to achieve this, they need to be insulin sensitive and produce an optimal amount of VEGF-A. In other tissues, insulin has been shown to regulate VEGF-A release, but this has not been previously examined in the podocyte. Using in vitro and in vivo approaches, in the present study, we now show that insulin regulates VEGF-A in the podocyte in both mice and humans via the insulin receptor (IR). Insulin directly increased VEGF-A mRNA levels and protein production in conditionally immortalized wild-type human and murine podocytes. Furthermore, when podocytes were rendered insulin resistant in vitro (using stable short hairpin RNA knockdown of the IR) or in vivo (using transgenic podocyte-specific IR knockout mice), podocyte VEGF-A production was impaired. Importantly, in vivo, this occurs before the development of any podocyte damage due to podocyte insulin resistance. Modulation of VEGF-A by insulin in the podocyte may be another important factor in the development of glomerular disease associated with conditions in which insulin signaling to the podocyte is deranged. © 2013 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/195408
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHale, LJ-
dc.contributor.authorHurcombe, J-
dc.contributor.authorLay, A-
dc.contributor.authorSantamaría, B-
dc.contributor.authorValverde, AM-
dc.contributor.authorSaleem, MA-
dc.contributor.authorMathieson, PW-
dc.contributor.authorWelsh, GI-
dc.contributor.authorCoward, RJ-
dc.date.accessioned2014-02-28T06:12:06Z-
dc.date.available2014-02-28T06:12:06Z-
dc.date.issued2013-
dc.identifier.citationAmerican Journal of Physiology - Renal Physiology, 2013, v. 305 n. 2, p. F182-F188-
dc.identifier.issn0363-6127-
dc.identifier.urihttp://hdl.handle.net/10722/195408-
dc.description.abstractPodocytes are critically important for maintaining the integrity of the glomerular filtration barrier and preventing albuminuria. Recently, it has become clear that to achieve this, they need to be insulin sensitive and produce an optimal amount of VEGF-A. In other tissues, insulin has been shown to regulate VEGF-A release, but this has not been previously examined in the podocyte. Using in vitro and in vivo approaches, in the present study, we now show that insulin regulates VEGF-A in the podocyte in both mice and humans via the insulin receptor (IR). Insulin directly increased VEGF-A mRNA levels and protein production in conditionally immortalized wild-type human and murine podocytes. Furthermore, when podocytes were rendered insulin resistant in vitro (using stable short hairpin RNA knockdown of the IR) or in vivo (using transgenic podocyte-specific IR knockout mice), podocyte VEGF-A production was impaired. Importantly, in vivo, this occurs before the development of any podocyte damage due to podocyte insulin resistance. Modulation of VEGF-A by insulin in the podocyte may be another important factor in the development of glomerular disease associated with conditions in which insulin signaling to the podocyte is deranged. © 2013 the American Physiological Society.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiology-
dc.titleInsulin directly stimulates VEGF-A production in the glomerular podocyte-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajprenal.00548.2012-
dc.identifier.pmid23698113-
dc.identifier.scopuseid_2-s2.0-84880149950-
dc.identifier.volume305-
dc.identifier.issue2-
dc.identifier.spageF182-
dc.identifier.epageF188-
dc.identifier.isiWOS:000321822400005-
dc.identifier.f1000718503824-

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