Calmodulin‐like skin protein (CLSP) is a secreted peptide that is produced by skin keratinocytes and some related epithelial cells. It has previously been shown that CLSP is recruited via the bloodstream into the central nervous system where it likely exerts a neuroprotective effect against toxicity related to Alzheimer's disease (AD) by binding to the heterotrimeric humanin receptor and activating intracellular survival signaling. However, it remains to be elucidated whether secreted CLSP shows a protective effect in the skin tissues. In the current study, using primary keratinocytes treated with hydrogen peroxide (H2O2) or exposed to ultraviolet (UV) irradiation as senescence models of keratinocytes, we addressed whether CLSP affects senescence in skin keratinocytes. We found that CLSP expression was upregulated by H2O2 or UV in keratinocytes. Furthermore, co‐incubation with recombinant CLSP reduced the increase in senescence‐associated β‐galactosidase‐positivity in keratinocytes that were induced by H2O2 or UV. These results suggest that CLSP may function as a senescence‐suppressing factor in keratinocytes.
Calmodulin-like skin protein (CLSP) is a secreted peptide that is restrictedly produced in skin keratinocytes and some related epithelial cells. It has been previously shown that CLSP is recruited via blood stream into the central nervous system where it likely exerts neuroprotective effect against toxicity related to Alzheimer's disease (AD) by binding to the heterotrimeric humanin receptor and activates intracellular survival signaling. However, it remains to be elucidated whether secreted CLSP has some biological activities outside the central nervous system. In the current study, using hydrogen peroxide (H 2 O 2 ) -and ultraviolet (UV) -induced senescence models of primarily cultured skin keratinocytes, we have addressed to the question as to whether CLSP is involved in senescence of skin keratinocytes. We first found that CLSP expression was potentiated by the treatment with H 2 O 2 and the exposure to UV in keratinocytes. Furthermore, the co-incubation with recombinant CLSP reduces Senescence-associated betagalactosidase-positivity in keratinocytes that is induced by the treatment with H 2 O 2 and the exposure to UV. These results suggest that CLSP may function as a senescence-suppressing factor for keratinocytes.
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