Abstract
Cellular senescence is an irreversible growth arrest caused by oxidative stress and DNA damage and ultraviolet (UV) radiation mediated cellular damage is responsible for skin photoaging. Type 17 collagen (COL17) is crucial for preventing skin aging. Apocynin, a NADPH oxidase inhibitor can chemically induce COL17 protein synthesis and promote stem cell survival. Our unpublished data showed that klotho mutant (kl/kl) mice, which is a premature aging model, displayed increased senescence-associated-β-galactosidase (Sa-β-Gal) activity, increased production of p16, phosphorylated histone H2AX (γH2AX), matrix metallopeptidase 9 and 1 (MMP-9, MMP-1), increased activation of mitogen-activated kinase (MAPK) along with deceased COL17 production in the skin.
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