p38 Mitogen-activated protein kinase affects transforming growth factor-beta/Smad signaling in human dental pulp cells.

Abstract:

:Transforming Growth Factor-beta (TGF-beta) plays an essential role in differentiation of dental pulp cells into odontoblasts during reparative dentine formation. However, the mechanism by which TGF-beta stimulates dental repair remains rather obscure. Human dental pulp cells were used as an in vitro model in the present work. We showed that TGF-beta signaled through mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38, along with Smad pathway. Distinct pathways exerted different time response. SB203580, a specific p38 MAPK inhibitor, reduced phosphorylation of Smad3, while it slightly enhanced phosphorylation of Smad2. Increased phosphorylation of ERK1/2 and p38 confirmed that SB203580 did not block activation of TGF-beta receptors. In addition, the inhibition of ERK1/2 activity with MEK1/2 inhibitor U0126 increased TGF-beta mediated phosphorylation of Smad3. Our results suggest that p38 affects the phosphorylation of Smad2 and Smad3 differentially during TGF-beta signaling in human dental pulp cells and ERK1/2 might be involved in the process.

journal_name

Mol Cell Biochem

authors

Wang FM,Hu T,Tan H,Zhou XD

doi

10.1007/s11010-006-9193-8

subject

Has Abstract

pub_date

2006-10-01 00:00:00

pages

49-54

issue

1-2

eissn

0300-8177

issn

1573-4919

journal_volume

291

pub_type

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