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Paracrine crosstalk between endothelial cells and melanocytes through clusterin to inhibit pigmentation
Author(s) -
Kim Misun,
Lee Jiun,
Park Tae Jun,
Kang Hee Young
Publication year - 2018
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/exd.13443
Subject(s) - clusterin , paracrine signalling , microphthalmia associated transcription factor , microbiology and biotechnology , biology , crosstalk , endothelial stem cell , autocrine signalling , cell culture , apoptosis , transcription factor , in vitro , biochemistry , genetics , gene , physics , receptor , optics
Cutaneous vasculature systems play a role in regulating skin pigmentation. We analysed RNA sequencing data to identify novel antimelanogenic factors secreted from endothelial cells and found that one of the secreted factors, clusterin, is highly expressed by HDMEC s. To investigate the paracrine effect of clusterin from HDMEC s on the regulation of melanogenesis, HDMEC s were infected with clusterin or sh‐clusterin lentivirus and the HDMEC ‐derived conditioned media were used to treat normal human melanocytes. It was found that HDMEC ‐derived clusterin inhibits melanogenesis through MITF /tyrosinase downregulation. The findings here suggest that HDMEC s secrete copious amounts of clusterin and that the clusterin is a factor contributing to the inhibitory effect of endothelial cells on melanogenesis via paracrine crosstalk between endothelial cells and melanocytes.