Biomol Ther.  2017 Sep;25(5):511-518. 10.4062/biomolther.2017.119.

Aquatide Activation of SIRT1 Reduces Cellular Senescence through a SIRT1-FOXO1-Autophagy Axis

Affiliations
  • 1Department of Microbiology and Molecular Biology, School of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of Korea. jkahn@cnu.ac.kr
  • 2Peptide R&D Center, Incospharm Corporation, Daejeon 34055, Republic of Korea.
  • 3College of Pharmacy Chungbuk National University, Cheongju 28644, Republic of Korea.
  • 4Division of Biomedical Convergence and Institute of Bioscience & Biotechnology, Kangwon National University, Chuncheon 24341, Republic of Korea.
  • 5Gladstone Institute of Virology and Immunology, Gladstone Institute of Neurological Disease, School of Medicine, Department of Neurology, University of California, San Francisco, CA 94158, USA.
  • 6Department of Cosmetic Science, Seowon University, Cheongju 28674, Republic of Korea.
  • 7Korea Basic Science Institute, Cheongju 28119, Republic of Korea.
  • 8Radiation Biotechnology Research Division, Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 26212, Republic of Korea.
  • 9NeoPharm USA, Englewood Cliffs, NJ 07632, USA.
  • 10Department of Dermatology, School of Medicine, University of California, San Francisco, and Northern California Institute for Research and Education, Veterans Affairs Medical Center, San Francisco, CA 94158, USA. Kyungho.Park@hallym.ac.kr
  • 11Department of Food Science and Nutrition, and Convergence Program of Material Science for Medicine and Pharmaceutics, Hallym University, Chuncheon 24252, Republic of Korea.

Abstract

Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by SA-β-gal staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.

Keyword

Cutaneous cellular senescence; UV irradiation; Aquatide; SIRT1; Autophagy

MeSH Terms

Autophagy
Cell Aging*
Fibroblasts
Humans
Skin
Skin Aging
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