PED/PEA-15 induces autophagy and mediates TGF-beta1 effect on muscle cell differentiation. (Articolo in rivista)

Type

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

Label

• PED/PEA-15 induces autophagy and mediates TGF-beta1 effect on muscle cell differentiation. (Articolo in rivista) (literal)

Anno

• 2012-01-01T00:00:00+01:00 (literal)

Alternative label

• Iovino S, Oriente F, Botta G, Cabaro S, Iovane V, Paciello O, Viggiano D, Perruolo G, Formisano P, Beguinot F. (2012)
  PED/PEA-15 induces autophagy and mediates TGF-beta1 effect on muscle cell differentiation.
  in Cell death and differentiation
  (literal)

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

• Iovino S, Oriente F, Botta G, Cabaro S, Iovane V, Paciello O, Viggiano D, Perruolo G, Formisano P, Beguinot F. (literal)

Rivista

• Cell death and differentiation (Rivista)

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

• Istituto di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Via Pansini 5, 80131 Napoli, Italy. Department of Cellular and Molecular Biology and Pathology, University of Naples Federico II, Italy. (literal)

Titolo

• PED/PEA-15 induces autophagy and mediates TGF-beta1 effect on muscle cell differentiation. (literal)

Abstract

• TGF-beta1 has been shown to induce autophagy in certain cells but whether and how this action is exerted in muscle and whether this activity relates to TGF-beta1 control of muscle cell differentiation remains unknown. Here, we show that expression of the autophagy-promoting protein phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes (PED/PEA-15) progressively declines during L6 and C2C12 skeletal muscle cell differentiation. PED/PEA-15 underwent rapid induction upon TGF-beta1 exposure of L6 and C2C12 myoblasts, accompanied by impaired differentiation into mature myotubes. TGF-beta1 also induced autophagy in the L6 and C2C12 cells through a PP2A/FoxO1-mediated mechanism. Both the TGF-beta1 effect on differentiation and that on autophagy were blocked by specific PED/PEA-15 ShRNAs. Myoblasts stably overexpressing PED/PEA-15 did not differentiate and showed markedly enhanced autophagy. In these same cells, the autophagy inhibitor 3-methyladenine rescued TGF-beta1 effect on both autophagy and myogenesis, indicating that PED/PEA-15 mediates TGF-beta1 effects in muscle. Muscles from transgenic mice overexpressing PED/PEA-15 featured a significant number of atrophic fibers, accompanied by increased light chain 3 (LC3)II to LC3I ratio and reduced PP2A/FoxO1 phosphorylation. Interestingly, these mice showed significantly impaired locomotor activity compared with their non-transgenic littermates. TGF-beta1 causes transcriptional upregulation of the autophagy-promoting gene PED/PEA-15, which in turn is capable to induce atrophic responses in skeletal muscle in vivo. (literal)

Prodotto di

• 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)

Autore CNR

• FRANCESCO BEGUINOT (Unità di personale esterno)
• PIETRO FORMISANO (Persona)
• Giuseppe Perruolo (Unità di personale esterno)

Incoming links:

Autore CNR di

• FRANCESCO BEGUINOT (Unità di personale esterno)
• PIETRO FORMISANO (Persona)
• Giuseppe Perruolo (Unità di personale esterno)

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

• Cell death and differentiation (Rivista)