Linked Life Data

15872077

Source:http://linkedlifedata.com/resource/pubmed/id/15872077

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pubmed-article:15872077pubmed:abstractTextPDGF and nitric oxide (NO) have been shown to participate in the progression of several forms of glomerulonephritis. A potential influence of NO on PDGF-mediated signaling cascades was therefore examined. Treatment of rat mesangial cells (MC) with the NO donors diethylenetriamine NO (DETA-NO) or spermine-NONOate resulted in a time- and dose-dependent upregulation of PDGF receptor alpha (PDGFRalpha) but not PDGFRbeta mRNA levels. Administration of DETA-NO also induced PDGFRalpha protein expression that was paralleled also by an enhanced receptor phosphorylation. Further experiments using 3-(5-hydroxymethyl-2-furyl)-1-benzylindazole (YC-1), an activator of the soluble guanylyl cyclase (sGC), the membrane-soluble cyclic GMP (cGMP) analog 8-Bromo-PET-cGMP, and the inhibitors of sGC ODQ and NS2028 suggest that elevated cGMP levels are responsible for the effects of NO. Importantly, NO-dependent autophosphorylation of PDGFRalpha drastically augmented PDGF-AA-evoked phosphorylation of PKB/Akt, a classical downstream target of PDGFRalpha signaling. Furthermore, in a rat model of anti-Thy-1 glomerulonephritis, expression and phosphorylation of PDGFRalpha but not PDGFRbeta expression was markedly reduced in nephritic animals that were treated with the inducible NO synthase inhibitor L-N6(1-iminoethyl)lysine(dihydrochloride) (L-NIL) compared with non-L-NIL-treated nephritic rats as demonstrated by Western blotting and immunohistochemistry. Taken together, the data suggest that NO modulates PDGFRalpha-triggered signaling in a cGMP-dependent manner by induction of PDGFRalpha expression in MC and in a rat model of mesangioproliferative glomerulonephritis. The mechanistic details of this regulation have to be elucidated in further experiments.lld:pubmed
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pubmed-article:15872077pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:15872077pubmed:articleTitleNitric oxide upregulates induction of PDGF receptor-alpha expression in rat renal mesangial cells and in anti-Thy-1 glomerulonephritis.lld:pubmed
pubmed-article:15872077pubmed:affiliationPharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe Universität Frankfurt am Main, Theodor-Stern-Kai 7, D-60590, Frankfurt am Main, Germany. k.f.beck@em.uni-frankfurt.delld:pubmed
pubmed-article:15872077pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15872077pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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