Nutr Res Pract.  2022 Feb;16(1):1-13. 10.4162/nrp.2022.16.1.1.

Bitter taste receptors protect against skin aging by inhibiting cellular senescence and enhancing wound healing

Affiliations
  • 1Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea
  • 2Interdisciplinary Program in Bioengineering, Seoul National University, Seoul 08826, Korea
  • 3School of Chemical and Biological Engineering, Institute of Chemical Processes, Seoul National University, Seoul 08826, Korea

Abstract

BACKGROUND/OBJECTIVES
Bitter taste receptors are taste signaling pathway mediators, and are also expressed and function in extra-gustatory organs. Skin aging affects the quality of life and may lead to medical issues. The purpose of this study was to better understand the anti-skin aging effects of bitter taste receptors in D-galactose (D-gal)-induced aged human keratinocytes, HaCaT cells.
MATERIALS/METHODS
Expressions of bitter taste receptors in HaCaT cells and mouse skin tissues were examined by polymerase chain reaction assay. Bitter taste receptor was overexpressed in HaCaT cells, and D-gal was treated to induce aging. We examined the effects of bitter taste receptors on aging by using β-galactosidase assay, wound healing assay, and Western blot assay.
RESULTS
TAS2R16 and TAS2R10 were expressed in HaCaT cells and were upregulated by D-gal treatment. TAS2R16 exerted protective effects against skin aging by regulating p53 and p21, antioxidant enzymes, the SIRT1/mechanistic target of rapamycin pathway, cell migration, and epithelial-mesenchymal transition markers. TAS2R10 was further examined to confirm a role of TAS2R16 in cellular senescence and wound healing in D-gal-induced aged HaCaT cells.
CONCLUSIONS
Our results suggest a novel potential preventive role of these receptors on skin aging by regulating cellular senescence and wound healing in human keratinocyte, HaCaT.

Keyword

Taste; galactose; skin aging; wound healing; keratinocytes
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