Induction of Type 17 Collagen Decreases Ultraviolet B-Induced Cellular Senescence in Human hTert/KER-CT Keratinocytes
TLDR Increasing type 17 collagen reduces aging signs in skin cells caused by UV light.
The study investigates the role of Type 17 collagen (COL17A1) in reducing cellular senescence caused by Ultraviolet B (UVB) radiation. Cellular senescence, an irreversible growth arrest, is a significant factor in skin photoaging. The chemical inducer Apocynin was used to promote COL17A1 protein synthesis in hTert/KER-CT keratinocytes. The results showed that UVB exposure decreased COL17A1 expression, increased senescence markers (Sa-β-Gal activity, p16 expression, and γH2AX expression), and caused cell cycle arrest. However, pretreatment with Apocynin restored COL17A1 expression and reduced senescence, cell cycle arrest, and the expression of γH2AX and p16. This suggests that Apocynin, by restoring COL17A1 expression under UVB stress, may maintain epidermal stem cell functionality, reduce senescence, and decrease DNA damage. The exact mechanism remains unclear.
