title: Influence of trichloroacetic acid peeling on the skin stress response system.
abstract: Although trichloroacetic acid (TCA) peeling is widely applied for cosmetic treatment of photodamaged skin, the entire biological mechanisms have yet to be determined. The skin stress response system (SSRS) involves corticotropin-releasing hormone (CRH) and proopiomelanocortin (POMC) products that are locally-generated in response to locally-provided stressors or pro-inflammatory cytokines. This system would restrict tissue damage and restore local homeostasis. To determine the influence of TCA peeling on the SSRS in vitro and in vivo, expressions of POMC, melanocortin receptor 1 (MC1R), CRH and CRH receptor 1 (CRHR1) mRNA were examined by reverse transcription polymerase chain reaction in Pam212 murine keratinocytes, murine plantar and healthy human abdominal skin specimens after TCA treatment. In addition, their protein expressions as well as those of POMC-derived peptides were examined immunohistochemically. After TCA treatment, transient upregulation of POMC and MC1R mRNA expressions was observed in both murine and human skin, as well as in Pam212. Enhanced POMC protein, recovery of once-impaired MC1R protein, and no enhancement of POMC-derived peptide productions were revealed immunohistochemically in both murine and human epidermis. In contrast, neither expression levels of CRH and CRHR1 mRNA nor epidermal protein were enhanced after TCA application in murine and human skin, except for induction of human CRH mRNA expression. These results suggest that TCA activates the SSRS by inducing POMC and MC1R productions of keratinocytes in the CRH-independent manner, and that the biological effects of POMC itself are responsible for the TCA-induced epidermal SSRS activation.
authors.affiliation: Department of Dermatology, Wakayama Medical University, Wakayama, Japan. kimkim@wakayama-med.ac.jp
authors.forename: Ayako
authors.initials: A
authors.lastname: Kimura
authors.forename: Nobuo
authors.initials: N
authors.lastname: Kanazawa
authors.forename: Hong-Jin
authors.initials: HJ
authors.lastname: Li
authors.forename: Nozomi
authors.initials: N
authors.lastname: Yonei
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Fukumi
authors.initials: F
authors.lastname: Furukawa
mesh_terms: D000818:Animals; D002999:Clone Cells; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D007641:Keratolytic Agents / Q000008:administration & dosage / Q000633:toxicity*; D051379:Mice; D057507:Mice, 129 Strain; D008875:Middle Aged; D011333:Pro-Opiomelanocortin / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D044102:Receptor, Melanocortin, Type 1 / Q000235:genetics / Q000378:metabolism; D018019:Receptors, Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000378:metabolism; D013312:Stress, Physiological / Q000187:drug effects; D014238:Trichloroacetic Acid / Q000008:administration & dosage / Q000633:toxicity*; D000099052:CRF Receptor, Type 1
chemical_list: D007641:Keratolytic Agents; D012333:RNA, Messenger; D044102:Receptor, Melanocortin, Type 1; D018019:Receptors, Corticotropin-Releasing Hormone; D000099052:CRF Receptor, Type 1; D014238:Trichloroacetic Acid; D011333:Pro-Opiomelanocortin; D003346:Corticotropin-Releasing Hormone