Periostin in the pathogenesis of skin diseases

Cell Mol Life Sci. 2017 Dec;74(23):4321-4328. doi: 10.1007/s00018-017-2647-1. Epub 2017 Sep 15.

Abstract

Skin is an organ that is susceptible to damage by external injury, chronic inflammation, and autoimmunity. Tissue damage causes alterations in both the configuration and type of cells in lesional skin. This phenomenon, called tissue remodeling, is a universal biological response elicited by programmed cell death, inflammation, immune disorders, and tumorigenic, tumor proliferative, and cytoreductive activity. In this process, changes in the components of the extracellular matrix are required to provide an environment that facilitates tissue remodeling. Among these extracellular matrix components, periostin, a glycoprotein that is predominantly secreted from dermal fibroblasts, has attracted attention. Periostin localizes in the papillary dermis of normal skin, and is aberrantly expressed in the dermis of lesional skin in atopic dermatitis, scar, systemic/limited scleroderma, melanoma, cutaneous T cell lymphoma, and skin damage caused by allergic/autoimmune responses. Periostin induces processes that result in the development of dermal fibrosis, and activate or protract the immune response. The aim of this review was to summarize recent knowledge of the role of periostin in the pathogenesis of dermatoses, and to explore whether periostin is a potential therapeutic target for skin diseases.

Keywords: Atopic dermatitis; Melanoma; Mycosis fungoides; Periostin; Scar; Scleroderma; Skin diseases.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Adhesion Molecules / genetics*
  • Cell Adhesion Molecules / immunology
  • Cell Differentiation
  • Collagen Type I / genetics
  • Collagen Type I / immunology
  • Cytokines / genetics
  • Cytokines / immunology
  • Dermatitis, Atopic / genetics*
  • Dermatitis, Atopic / immunology
  • Dermatitis, Atopic / pathology
  • Extracellular Matrix / immunology
  • Extracellular Matrix / pathology
  • Fibroblasts / immunology
  • Fibroblasts / pathology*
  • Fibrosis
  • Gene Expression Regulation
  • Humans
  • Inflammation
  • Melanoma / genetics*
  • Melanoma / immunology
  • Melanoma / pathology
  • Scleroderma, Systemic / genetics*
  • Scleroderma, Systemic / immunology
  • Scleroderma, Systemic / pathology
  • Signal Transduction
  • Skin / immunology
  • Skin / pathology
  • Skin Neoplasms / genetics*
  • Skin Neoplasms / immunology
  • Skin Neoplasms / pathology

Substances

  • Cell Adhesion Molecules
  • Collagen Type I
  • Cytokines
  • POSTN protein, human