14:00 - 15:50
Thu-Park Suites-N
Park Suites
Poster Session
A study on the cellular senescence-inducing function of aging markers acting on the 1st aging peak.
302
Presented by: Soyoun Lee
Soyoun Lee 1, Hongyan An 1, Hang Woong Park 1, Jinhun Cho 2
1 Skin Science Research Center, NewLife Bio Science Technology Co.,Ltd., Seoul
2 New Life Cosmetics R&D Center Co., Ltd., Shanghai
The final goal of cosmetic research is to prevent skin aging and restore aging skin. As part of this effort, in a previous study, we discovered four types of aging marker genes, FSTL3, GDF15, MMP12, and CCDC80, whose expression in skin cells changes significantly during the 1st aging peak that occurs around the age of 40. MMP12 as an elastase was confirmed to increase with aging of skin cells, and it can promote the degradation of elastin in the skin and cause a decrease in skin elasticity. However, in the case of FSTL3, GDF15 and CCDC80, except for MMP12 among the four aging markers, what function induces skin aging is not yet known. So, we conducted a study to elucidate the mechanism by which these four aging markers cause skin aging.
SA-β-gal activity was measured in recombinant protein-treated skin cells to evaluate whether the senescence of the cells in accelerated by the aging markers. In addition, we evaluated the change in SA-β-Gal activity when the expression of aging markers was knocked down in the UV-induced senescence cell. The fluorescence of DCFDA staining was explored to confirm whether ROS was induced by the recombinant protein of aging markers. It was attempted to find a signal pathway that induces cellular senescence by inducing such ROS. In addition, it was checked whether skin melanin synthesis and glycation were promoted by aging markers.
The recombinant protein of the aging marker strongly promotes skin senescence. The aging marker's protein was increased the SA-β-gal activity of skin cells and induced ROS generation. This ROS generation is induced by the p16 pathway, and when the expression of aging markers was suppressed, it was confirmed that ROS generation and SA-β-gal activity of skin cells decreased, thereby inhibiting skin cell senescence. In addition, recombinant protein of the aging marker promotes melanin synthesis in melanocytes and glycation in skin cells.
We developed a technology to dramatically prevent aging by using aging markers that act during the 1st aging peak, when the skin is rapidly aging. We found that the skin aging marker promotes cell senescence by inducing ROS generation through the p16 signaling pathway. In addition, it was confirmed that melanin production and glycation that darken the skin tone were promoted by the aging marker. Through this, the aging markers we discovered can be used as a new target for the development of materials that can comprehensively care for skin aging in various fields, from wrinkles and elasticity to whitening and cellular senescence.