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Decreased Calcium-Sensing Receptor Expression Controls Calcium Signaling and Cell-To-Cell Adhesion Defects in Aged

Anna Celli1, Chia-Ling Tu2, Elise Lee1

  • 1Department of Dermatology, SFVAHCS Medical Center and University of California San Francisco, San Francisco, California, USA.

The Journal of Investigative Dermatology
|April 16, 2021
PubMed

Insights

Decreased calcium-sensing receptor (CaSR) expression impairs skin barrier function in aged individuals. Restoring CaSR function may offer a therapeutic approach for aging skin.

Area of Science:

  • Dermatology
  • Cell Biology
  • Calcium Signaling

Background:

  • The calcium-sensing receptor (CaSR) is crucial for epidermal homeostasis, regulating calcium ion (Ca2+) and E-cadherin functions.
  • Age-related decline in CaSR expression impacts skin barrier integrity and cellular communication.

Purpose of the Study:

  • To investigate the role of CaSR in age-related changes in epidermal calcium (Ca2+) signaling and E-cadherin organization.
  • To explore therapeutic strategies for restoring CaSR function in aging skin.

Main Methods:

  • Comparative analysis of CaSR expression and Ca2+ signaling in young and aged mouse epidermis and human keratinocytes.
  • Assessment of E-cadherin, phospholipase C-γ, and STIM1 expression.
  • Experimental wounding and CaSR agonist treatment to evaluate functional recovery.

Main Results:

  • Aged epidermis and keratinocytes exhibit reduced CaSR expression, impaired Ca2+ signal propagation, and altered Ca2+ homeostasis.
  • Decreased CaSR correlates with reduced E-cadherin and phospholipase C-γ, and increased STIM1.
  • CaSR agonist treatment normalized Ca2+ propagation and E-cadherin organization post-wounding.

Conclusions:

  • Age-related CaSR downregulation disrupts keratinocyte and epidermal Ca2+ signaling, impairing E-cadherin function and skin barrier homeostasis.
  • Restoring CaSR function presents a potential therapeutic avenue for age-related skin dysfunction.

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