The Polyamine Putrescine Promotes Human Epidermal Melanogenesis.
Biogenic Polyamines
/ metabolism
Cells, Cultured
Dicarboxylic Acid Transporters
/ physiology
Epidermis
/ drug effects
Humans
Melanins
/ biosynthesis
Melanocytes
/ drug effects
Middle Aged
Mitochondrial Membrane Transport Proteins
/ physiology
Putrescine
/ analogs & derivatives
Skin Pigmentation
/ drug effects
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
06
05
2019
revised:
17
01
2020
accepted:
03
02
2020
pubmed:
3
3
2020
medline:
7
4
2021
entrez:
3
3
2020
Statut:
ppublish
Résumé
Hyperpigmentary conditions can arise when melanogenesis in the epidermis is misregulated. Understanding the pathways underlying melanogenesis is essential for the development of effective treatments. Here, we report that a group of metabolites called polyamines are important in the control of melanogenesis in human skin. Polyamines are cationic molecules present in all cells and are essential for cellular function. We report that polyamine regulator ODC1 is upregulated in melanocytes from melasma lesional skin. We report that the polyamine putrescine can promote pigmentation in human skin explants and primary normal human epidermal melanocytes through induction of tyrosinase which is rate-limiting for the synthesis of melanin. Putrescine supplementation on normal human epidermal melanocytes results in the activation of polyamine catabolism, which results in increased intracellular H
Identifiants
pubmed: 32119868
pii: S0022-202X(20)30219-0
doi: 10.1016/j.jid.2020.02.009
pii:
doi:
Substances chimiques
Biogenic Polyamines
0
Dicarboxylic Acid Transporters
0
Melanins
0
Mitochondrial Membrane Transport Proteins
0
SLC25A21 protein, human
0
MDL 72527
1YVR349GN4
Putrescine
V10TVZ52E4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2032-2040.e1Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.