Perspective

Journal of Investigative Dermatology (2008) 128, 783–790. doi:10.1038/sj.jid.5700969

The Role of Smads in Skin Development

Philip Owens1,2,3, Gangwen Han1,2,3, Allen G Li1,2,3 and Xiao-Jing Wang1,2,3

  1. 1Department of Otolaryngology, Oregon Health Sciences University, Portland Oregon, USA
  2. 2Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland Oregon, USA
  3. 3Department of Dermatology, Oregon Health Sciences University, Portland Oregon, USA

Correspondence: Dr Xiao-Jing Wang, VAMC Building 103, Room F-221, 3710 SW US Veterans Hospital Road, Mail code R&D46, Portland, Oregon 97239, USA. E-mail: wangxiao@ohsu.edu

Received 12 February 2007; Revised 10 April 2007; Accepted 15 April 2007.

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Abstract

Smads are a group of signaling mediators and antagonists of the transforming growth factor-beta (TGF-beta) superfamily, responding but not limited to signaling from TGF-beta, Activin, and bone morphogenetic proteins (BMPs). As all of these three signaling pathways play important roles in skin development, we have been actively pursuing studies assessing the role of Smads in skin development. Our studies revealed that Smad-4 affects hair follicle differentiation primarily by mediating BMP signaling. Smad-7 significantly affects hair follicle development and differentiation by blocking the TGFbeta/Activin/BMP pathway and by inhibiting WNT/beta-catenin signaling via ubiquitin-mediated beta-catenin degradation. In contrast, other Smads may have redundant or dispensable functions in skin development. Here, we review the work that shows the emergence of Smad functions in skin development via traditional and novel signaling pathways.

Abbreviations:

ALK, activin-like kinase; BMP, bone morphogenetic protein; FGF, fibroblast growth factor; IRS, inner root sheath; R-Smad, receptor-specific Smad; Co-Smad, common partner Smad; I-Smad, inhibitory Smad; SHH, sonic Hedgehog; TGF-beta, transforming growth factor-beta

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