Overproduction of phosphoprotein enriched in diabetes (PED) induces mesangial expansion and upregulates protein kinase C-² activity and TGF-²1 expression. (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Overproduction of phosphoprotein enriched in diabetes (PED) induces mesangial expansion and upregulates protein kinase C-² activity and TGF-²1 expression. (Articolo in rivista) (literal)

Anno

• 2009-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

• 10.1007/s00125-009-1528-z (literal)

Alternative label

• Oriente F; Iovino S; Cassese A; Romano C; Miele C; Troncone G; Balletta M; Perfetti A; Santulli G; Iaccarino G; Valentino R; Beguinot F; Formisano P (2009)
  Overproduction of phosphoprotein enriched in diabetes (PED) induces mesangial expansion and upregulates protein kinase C-² activity and TGF-²1 expression.
  in Diabetologia (Berl.); SPRINGER, 233 SPRING ST, NEW YORK, NY 10013 (Stati Uniti d'America)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Oriente F; Iovino S; Cassese A; Romano C; Miele C; Troncone G; Balletta M; Perfetti A; Santulli G; Iaccarino G; Valentino R; Beguinot F; Formisano P (literal)

Pagina inizio

• 2642 (literal)

Pagina fine

• 2652 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 52 (literal)

Rivista

• Diabetologia (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

• 11 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

• 12 (literal)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• Department of Cellular and Molecular Biology and Pathology, Federico II University of Naples, Via Pansini 5, 80131 Naples, Italy Istituto di Endocrinologia ed Oncologia Sperimentale del C.N.R., Federico II University of Naples, Naples, Italy Department of Biomorphological and Functional Sciences, Federico II University of Naples, Italy Department of Nephrology, Federico II University of Naples, Naples, Italy Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University of Naples, Naples, Italy (literal)

Titolo

• Overproduction of phosphoprotein enriched in diabetes (PED) induces mesangial expansion and upregulates protein kinase C-² activity and TGF-²1 expression. (literal)

Abstract

• Aims/hypothesis Overproduction of phosphoprotein enriched in diabetes (PED, also known as phosphoprotein enriched in astrocytes-15 [PEA-15]) is a common feature of type 2 diabetes and impairs insulin action in cultured cells and in mice. Nevertheless, the potential role of PED in diabetic complications is still unknown. Methods We studied the effect of PED overproduction and depletion on kidney function in animal and cellular models. Results Transgenic mice overexpressing PED (PEDTg) featured age-dependent increases of plasma creatinine levels and urinary volume, accompanied by expansion of the mesangial area, compared with wild-type littermates. Serum and kidney levels of TGF-?1 were also higher in 6- and 9-month-old PEDTg. Overexpression of PED in human kidney 2 cells significantly increased TGF-?1 levels, SMAD family members (SMAD)2/3 phosphorylation and fibronectin production. Opposite results were obtained following genetic silencing of PED in human kidney 2 cells by antisense oligonucleotides. Inhibition of phospholipase D and protein kinase C-? by 2-butanol and LY373196 respectively reduced TGF-?1, SMAD2/3 phosphorylation and fibronectin production. Moreover, inhibition of TGF-?1 receptor activity and SMAD2/3 production by SB431542 and antisense oligonucleotides respectively reduced fibronectin secretion by about 50%. TGF-?1 circulating levels were significantly reduced in Ped knockout mice and positively correlated with PED content in peripheral blood leucocytes of type 2 diabetic patients. Conclusions/interpretation These data indicate that PED regulates fibronectin production via phospholipaseD/protein kinase C-? and TGF-?1/SMAD pathways in kidney cells. Raised PED levels may therefore contribute to the abnormal accumulation of extracellular matrix and renal dysfunction in diabetes. (literal)

Editore

• SPRINGER, 233 SPRING ST (Editore)

Prodotto di

• Studio dell'espressione e della funzione di geni e proteine coinvolte nel diabete di tipo 2 (SV.P16.001.002) (Modulo)
• Istituto per l'endocrinologia e l'oncologia \"Gaetano Salvatore\" (IEOS) (Istituto)

Autore CNR

• PIETRO FORMISANO (Persona)
• FRANCESCO BEGUINOT (Unità di personale esterno)
• CLAUDIA MIELE (Persona)
• ROSSELLA VALENTINO (Persona)

Incoming links:

Autore CNR di

• ROSSELLA VALENTINO (Persona)
• FRANCESCO BEGUINOT (Unità di personale esterno)
• CLAUDIA MIELE (Persona)
• PIETRO FORMISANO (Persona)

Prodotto

• Istituto per l'endocrinologia e l'oncologia \"Gaetano Salvatore\" (IEOS) (Istituto)
• Studio dell'espressione e della funzione di geni e proteine coinvolte nel diabete di tipo 2 (SV.P16.001.002) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Diabetologia (Rivista)

Editore di

• SPRINGER, 233 SPRING ST (Editore)