Loss of Smad3 modulates wound healing.

Abstract:

:TGF-beta plays a central and critical role in tissue repair. The recent identification of TGF-beta signal transduction pathways involving Smad proteins has now made it possible to explore their contribution to the activities of TGF-beta in vivo. Both Smad3 and its closely related homolog Smad2 act as latent nuclear transcriptional activators and mediate intracellular signaling by TGF-betas and activin, each of which regulates cellular functions pivotal to cutaneous wound healing. Mice null for Smad3 (Smad3(ex8/ex8)) survive into adulthood and show accelerated cutaneous wound healing characterized by an increased rate of re-epithelialization and a reduced local inflammatory infiltrate. These data implicate Smad3 in specific pathways of tissue repair and suggest that it could be a target for the development of therapeutic strategies to modulate wound healing.

authors

Ashcroft GS,Roberts AB

doi

10.1016/s1359-6101(99)00036-2

subject

Has Abstract

pub_date

2000-03-01 00:00:00

pages

125-31

issue

1-2

eissn

1359-6101

issn

1879-0305

pii

S1359-6101(99)00036-2

journal_volume

11

pub_type

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