TMEM207-mediated the impairment of skin regeneration through YAP sequestration in an allergic contact dermatitis

Shusuke Nomura1, Yusuke Kito1, Chiemi Saigo1

  • 1Department of Pathology and Translational Research, Gifu University Graduate School of Medicine, Yanagido 1-1, Gifu, 501-1194, Japan.

Abstract

Insights

Abnormal Transmembrane protein 207 (TMEM207) expression impairs skin regeneration by affecting the Yes-associated protein (YAP) pathway. This exacerbates allergic contact dermatitis, highlighting TMEM207

Area of Science:

  • Dermatology and Molecular Biology
  • Cellular Biology and Regenerative Medicine

Background:

  • The Yes-associated protein (YAP) is crucial for cell proliferation and skin homeostasis.
  • YAP plays a significant role in stem/progenitor cell function, cancer, and wound healing.
  • Allergic contact dermatitis involves impaired skin regeneration.

Purpose of the Study:

  • To investigate the role of Transmembrane protein 207 (TMEM207) in allergic contact dermatitis.
  • To explore the YAP-mediated regulation of TMEM207 in atopic models.
  • To understand how TMEM207 influences skin regeneration and disease severity.

Main Methods:

  • Investigated TMEM207 expression and pathological characteristics in atopic models.
  • Utilized immunoprecipitation to confirm binding between TMEM207 and YAP.
  • Employed immunohistochemical staining to assess YAP nuclear localization.

Main Results:

  • TMEM207 was detected in mouse sebaceous glands and hair roots.
  • TMEM207 binds to YAP, and its abnormal expression leads to decreased YAP nuclear localization.
  • Reduced expression of ATP binding cassette subfamily B member 1 (ABCB1) and MIB E3 Ubiquitin Protein Ligase 1 (MIB-1) was observed.

Conclusions:

  • Abnormal TMEM207 expression contributes to reduced skin regeneration capacity.
  • YAP dysregulation mediated by TMEM207 aggravates allergic contact dermatitis.
  • TMEM207 is a potential therapeutic target for improving skin regeneration in allergic contact dermatitis.