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Influence of chemical peeling on the skin stress response system
Author(s) -
Kimura Ayako,
Kanazawa Nobuo,
Li HongJin,
Yonei Nozomi,
Yamamoto Yuki,
Furukawa Fukumi
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2012.01495.x
Subject(s) - proopiomelanocortin , adrenocorticotropic hormone , proinflammatory cytokine , melanocyte stimulating hormone , hormone , trichloroacetic acid , inflammation , stressor , human skin , corticotropin releasing hormone , homeostasis , endocrinology , medicine , chemistry , biology , biochemistry , neuroscience , genetics
Skin stress response system (SSRS) involves corticotropin‐releasing hormone (CRH) and proopiomelanocortin (POMC)‐derived peptides, such as adrenocorticotropic hormone (ACTH), a‐melanocyte‐stimulating hormone (MSH) and b‐endorphin that are locally generated in response to locally provided stressors or proinflammatory cytokines. This system would restrict tissue damage and restore local homoeostasis. Trichloroacetic acid (TCA) is one of the most widely used peeling agents and applied for cosmetic treatment of photodamaged skin. However, the biological mechanism responsible for TCA peeling has yet to be fully determined. While our investigation focused on the inflammation and wound healing pathways, in the recent study, we have examined involvement of the SSRS as the third pathway. Mostly depending on our findings that TCA peeling activates the SSRS by inducing the POMC expression of keratinocytes in the CRH‐independent manner, together with the results reported by other researchers, we can say that the biological effect of POMC seems to be responsible for the TCA‐induced epidermal SSRS activation.