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IL-13 Promotes the Proliferation of Rat Pancreatic Stellate Cells Through the Suppression of NF-kappaB/TGF-beta1 Pathway

IL-13 Promotes the Proliferation of Rat Pancreatic Stellate Cells Through the Suppression of NF-kappaB/TGF-beta1 Pathway

Satoshi Shinozaki, Hirosato Mashima, Hirohide Ohnishi, Kentaro Sugano

Biochem Biophys Res Commun. 2010 Feb 26;393(1):61-5.

PMID: 20100461

Abstract:

In chronic pancreatitis, pancreatic stellate cells (PSCs) play a central role in tissue fibrogenesis. Transforming growth factor beta(1) (TGF-beta(1)) and the Th2 lymphokines such as interleukin (IL)-13 are major profibrogenic cytokines in many organs. Activated PSCs produce various inflammatory cytokines including TGF-beta(1). In this study, we investigated whether IL-13 affects pancreatic fibrogenesis by modulating the functions of PSCs. IL-13 promoted PSCs proliferation without activation through the suppression of autocrine TGF-beta(1). IL-13 enhanced Stat6 phosphorylation in PSCs but Stat6 was not involved in the suppression of TGF-beta(1). IL-13 inhibited the transcriptional activity of NF-kappaB, and the expression of mutant I-kappaB reproduced the suppression of autocrine TGF-beta(1) and promoted PSCs proliferation. Taken together, we demonstrated that IL-13 promotes PSCs proliferation through the suppression of the transcriptional activity of NF-kappaB, resulting in the decrease of autocrine TGF-beta(1). This finding provides an unequivocal evidence of IL-13 participation in pancreatic fibrosis, illustrating a new strategy for chronic pancreatitis.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413351	IL-13 from rat			Price

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