583 Induction of type 17 collagen decreases ultraviolet b-induced cellular senescence in human htert/ker-ct keratinocytes

Cellular senescence is an irreversible growth arrest caused by oxidative stress and DNA damage ultraviolet radiation mediated cellular responsible for skin photoaging. The Type 17 collagen (COL17A1) expressed in epithelial hemidesmosomes plays a crucial role maintaining hair follicle stem cells. Apocynin, (1-(4-Hydroxy-3-methoxyphenyl)ethan-1-one)) chemical inducer of Collagen 17A1 which promotes the protein synthesis. Our unpublished data showed that klotho mutant (kl/kl) mice, premature aging model, display increased associated-β-galactosidase (Sa-β-Gal) activity, p16 phosphorylated histone H2AX (γH2AX) expression along with deceased expression. Here, we aimed to study whether induction COL17A1 apocynin can decrease Ultraviolet B (UVB)- induced cell or not. hTert/KER-CT keratinocytes were pretreated (10 μM, 20 40 μM) 24 hours exposed UVB (100 J/m2) using lamp. After 3 hours, COL17A1, p16, γH2AX was measured immunofluorescence qRT-PCR, SA-β-gal staining, propidium iodide (PI)/RNase solution used measure cycle analysis. In our study, exposure decreased epidermal basal cells, Sa-β-Gal G1 arrest, expression, (P<0.001). Apocynin restored reduced senescence, human Although mechanism not yet understood, speculate restores under thus maintain functionality. By cell’s homeostasis may also reduce damage.