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RGS::GFP expression in endocrine pancreas during development and regeneration
Author(s) -
Wilkie Tom,
Villasenor Alethia,
Wang Zhao,
Hatten Mary E,
Scherer Philipp,
Cleaver Ondine
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.856.5
Subject(s) - biology , neogenesis , progenitor cell , enteroendocrine cell , microbiology and biotechnology , pancreas , endocrinology , medicine , islet , green fluorescent protein , embryonic stem cell , g protein coupled receptor , beta cell , signal transduction , stem cell , endocrine system , gene , insulin , genetics , hormone
Regulation of G protein signaling provides a promising approach for managing beta cell replication and neogenesis. RGS proteins are intracellular GTPase activating proteins (GAPs) that terminate ligand‐activated G protein coupled receptor (GPCR) signaling. We characterized expression of a GFP‐reporter gene integrated into two distinct RGS genes, Rgs8 and Rgs16, in embryonic and adult pancreas. Rgs16::GFP and Rgs8::GFP were expressed in pancreatic endocrine progenitor cells in embryos, neonates and weanlings but their expression was normally quiescent in adulthood. Rgs16 expression was reactivated in four different models of beta cell expansion: i) weanlings, ii) mid gestation pregnant females, iii) during islet regeneration in PANIC‐ATTAC mice, a model of type 1 diabetes and iv) in islets of obese, hyperglycemic ob/ob mice, a model of type 2 diabetes. Our results suggest that Rgs16 and Rgs8 control GPCR signaling during islet progenitor cell activation, differentiation, and beta cell expansion in embryos and metabolically stressed adults. Research support: NIGMS & Welch Foundation .