TRPV4 Moves toward Center-Fold in Rosacea Pathogenesis

J Invest Dermatol. 2017 Apr;137(4):801-804. doi: 10.1016/j.jid.2016.12.013.

Abstract

Mascarenhas et al. report that TRPV4 expression is upregulated in mast cells in response to the proteolytic cathelicidin fragment LL37 in a murine rosacea model and that TRPV4 loss of function attenuates mast cell degranulation. These findings render TRPV4 a translational-medical target in rosacea. However, signaling mechanisms causing increased expression of TRPV4 await elucidation. Moreover, we ask whether TRPV4-mediated Ca++-influx evokes mast cell degranulation.

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / metabolism*
  • Calcium Signaling / genetics
  • Cathelicidins
  • Cells, Cultured / cytology
  • Cells, Cultured / physiology
  • Disease Models, Animal
  • Humans
  • Mast Cells / cytology
  • Mast Cells / physiology
  • Mice
  • Rosacea / genetics*
  • Rosacea / physiopathology*
  • TRPV Cation Channels / genetics*
  • Translational Research, Biomedical
  • Up-Regulation / genetics

Substances

  • Antimicrobial Cationic Peptides
  • TRPV Cation Channels
  • TRPV4 protein, human
  • Cathelicidins