Selective Deletion of Pten in Pancreatic β Cells Leads to Increased Islet Mass and Resistance to STZ-Induced Diabetes

Author:

Stiles Bangyan L.1,Kuralwalla-Martinez Christine2,Guo Wei1,Gregorian Caroline1,Wang Ying1,Tian Jide1,Magnuson Mark A.3,Wu Hong1

Affiliation:

1. Molecular and Medical Pharmacology, UCLA David Geffen School of Medicine, Los Angeles, California

2. Department of Pediatrics, Division of Neonatology, Children's Hospital of Orange County, Orange, California

3. Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee

Abstract

ABSTRACT Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a lipid phosphatase. PTEN inhibits the action of phosphatidylinositol-3-kinase and reduces the levels of phosphatidylinositol triphosphate, a crucial second messenger for cell proliferation and survival, as well as insulin signaling. In this study, we deleted Pten specifically in the insulin producing β cells during murine pancreatic development. Pten deletion leads to increased cell proliferation and decreased cell death, without significant alteration of β-cell differentiation. Consequently, the mutant pancreas generates more and larger islets, with a significant increase in total β-cell mass. PTEN loss also protects animals from developing streptozotocin-induced diabetes. Our data demonstrate that PTEN loss in β cells is not tumorigenic but beneficial. This suggests that modulating the PTEN-controlled signaling pathway is a potential approach for β-cell protection and regeneration therapies.

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

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