TGFβ receptor signaling is essential for inflammation-induced but not β-cell workload-induced β-cell proliferation.

ABSTRACT: Protection and restoration of a functional β-cell mass are fundamental strategies for prevention and treatment of diabetes. Consequently, knowledge of signals that determine the functional β-cell mass is of immense clinical relevance. Transforming growth factor β (TGFβ) superfamily signaling pathways play a critical role in development and tissue specification. Nevertheless, the role of these pathways in adult β-cell homeostasis is not well defined. Here, we ablated TGFβ receptor I and II genes in mice undergoing two surgical β-cell replication models (partial pancreatectomy or partial duct ligation), representing two triggers for β-cell proliferation, increased β-cell workload and local inflammation, respectively. Our data suggest that TGFβ receptor signaling is necessary for baseline β-c

SUBMITTER: Xiao X 

PROVIDER: S-EPMC3609557 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature