STAT3 modulates β-cell cycling in injured mouse pancreas and protects against DNA damage.
Fiche publication
Date publication
juin 2016
Journal
Cell death & disease
Auteurs
Membres identifiés du Cancéropôle Est :
Dr GRADWOHL Gérard
Tous les auteurs :
De Groef S, Renmans D, Cai Y, Leuckx G, Roels S, Staels W, Gradwohl G, Baeyens L, Heremans Y, Martens GA, De Leu N, Sojoodi M, Van de Casteele M, Heimberg H
Lien Pubmed
Résumé
Partial pancreatic duct ligation (PDL) of mouse pancreas induces a doubling of the β-cell mass mainly through proliferation of pre-existing and newly formed β-cells. The molecular mechanism governing this process is still largely unknown. Given the inflammatory nature of PDL and inflammation-induced signaling via the signal transducer and activator of transcription 3 (STAT3), the activation and the role of STAT3 in PDL-induced β-cell proliferation were investigated. Duct ligation stimulates the expression of several cytokines that can act as ligands inducing STAT3 signaling and phosphorylation in β-cells. β-Cell cycling increased by conditional β-cell-specific Stat3 knockout and decreased by STAT3 activation through administration of interleukin-6. In addition, the level of DNA damage in β-cells of PDL pancreas increased after deletion of Stat3. These data indicate a role for STAT3 in maintaining a steady state in the β-cell, by modulating its cell cycle and protection from DNA damage.
Référence
Cell Death Dis. 2016 Jun;7(6):e2272