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Globular adiponectin acts as a melanogenic signal in human epidermal melanocytes
Author(s) -
Kim Y.,
Cho J.Y.,
Oh S.W.,
Kang M.,
Lee S.E.,
Jung E.,
Park Y.S.,
Lee J.
Publication year - 2018
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.16488
Subject(s) - globular cluster , melanosome , adiponectin , endocrinology , biology , medicine , anatomy , melanin , physics , genetics , astrophysics , insulin resistance , galaxy , insulin
Summary Background Adiponectin is an adipocyte‐derived cytokine that circulates as a full‐length protein and a fragment containing the globular domain of adiponectin ( gA d). A recent study has reported the antimelanogenic effects of full‐length adiponectin. Objectives To examine the involvement of gA d in melanogenesis and its mechanisms of action. Methods The effects of gA d on melanogenesis and its mechanisms of action were investigated in human epidermal melanocytes and reconstructed epidermis, including melanin content, cellular tyrosinase activity, cyclic adenosine monophosphate ( cAMP ) production and protein kinase A ( PKA ) activity, expression and phosphorylation of signalling molecules. Results Exogenous gA d increased melanin content, and the mRNA levels of microphthalmia‐associated transcription factor ( MITF ) and its downstream genes TRP 1 , but not TRP 2 , were increased by gA d. However, cAMP production and PKA activity were not affected by gA d. Moreover, attempts to elucidate the underlying mechanism behind the gA d‐mediated effect revealed that gA d could regulate melanogenesis by upregulating MITF through phosphorylation of the cAMP response element‐binding protein ( CREB ). In addition, upregulation of MITF was mediated by activation of adenosine monophosphate‐activated protein kinase ( AMPK )–p38 mitogen‐activated protein kinase ( MAPK ) signalling. Taken together, these findings indicate that promotion of melanogenesis by gA d occurs through increased expression of MITF , which is mediated by activation of the AMPK –p38 MAPK–CREB pathway. Conclusions These findings suggest that gA d contributes to epidermal homeostasis via its effect on melanocyte biology, and products of adipose tissue could affect epidermal biology.