Bitter taste receptors protect against skin aging by inhibiting cellular senescence and enhancing wound healing
- 주제(키워드) Taste , galactose , skin aging , wound healing , keratinocytes
- 주제(기타) Nutrition & Dietetics
- 설명문(일반) [Chung, Min Gi; Kim, Yerin; Kim, Yuri] Ewha Womans Univ, Dept Nutr Sci & Food Management, 52 Ewhayeodae Gil, Seoul 03760, South Korea; [Cha, Yeon Kyung; Park, Tai Hyun] Seoul Natl Univ, Interdisciplinary Program Bioengn, Seoul 08826, South Korea; [Park, Tai Hyun] Seoul Natl Univ, Sch Chem & Biol Engn, Inst Chem Proc, Seoul 08826, South Korea
- 등재 SCIE, SCOPUS, KCI등재
- OA유형 gold, Green Published
- 발행기관 KOREAN NUTRITION SOC
- 발행년도 2022
- URI http://www.dcollection.net/handler/ewha/000000190405
- 본문언어 영어
- Published As https://doi.org/10.4162/nrp.2022.16.1.1
- PubMed https://pubmed.ncbi.nlm.nih.gov/35116124
초록/요약
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 beta-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 ll-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.
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