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TOSO promotes β-cell proliferation and protects from apoptosis.

Abstract：

:Decreased β-cell mass reflects a shift from quiescence/proliferation into apoptosis, it plays a crucial role in the pathophysiology of diabetes. A major attempt to restore β-cell mass and normoglycemia is to improve β-cell survival. Here we show that switching off the Fas pathway using Fas apoptotic inhibitory protein (Faim/TOSO), which regulates apoptosis upstream of caspase 8, blocked β-cell apoptosis and increased proliferation in human islets. TOSO was clearly expressed in pancreatic β-cells and down-regulated in T2DM. TOSO expression correlated with β-cell turnover; at conditions of improved survival, TOSO was induced. In contrast, TOSO downregulation induced β-cell apoptosis. Although TOSO overexpression resulted in a 3-fold induction of proliferation, proliferating β-cells showed a very limited capacity to undergo multiple rounds of replication. Our data suggest that TOSO is an important regulator of β-cell turnover and switches β-cell apoptosis into proliferation.

journal_name

Mol Metab

journal_title

Molecular metabolism

authors

Dharmadhikari G,Mühle M,Schulthess FT,Laue S,Oberholzer J,Pattou F,Kerr-Conte J,Maedler K

doi

10.1016/j.molmet.2012.08.006

subject

Has Abstract

pub_date

2012-08-17 00:00:00

pages

70-8

issue

1-2

issn

2212-8778

pii

S2212-8778(12)00015-4

journal_volume

1

pub_type

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