Autophagy activators stimulate the removal of advanced glycation end products in human keratinocytes.
Journal
Journal of the European Academy of Dermatology and Venereology : JEADV
ISSN: 1468-3083
Titre abrégé: J Eur Acad Dermatol Venereol
Pays: England
ID NLM: 9216037
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
12
02
2020
revised:
04
03
2020
accepted:
27
03
2020
entrez:
20
6
2020
pubmed:
20
6
2020
medline:
30
4
2021
Statut:
ppublish
Résumé
The accumulation of advanced glycation end products (AGEs) can impact cellular homoeostasis and protein structure, thus is implicated in numerous skin conditions including yellow, dull appearance. AGE formation is irreversible; thus, understanding of the recycling process of AGEs in the skin is critical for addressing skin appearance conditions. To determine whether (i) accumulation of AGEs occurs in dull appearance group among young population (age 20-29) (ii) in vitro autophagy stimulation results in reduction of AGEs in keratinocytes. Facial cheek biopsies were collected from Chinese women (age 20-50) exhibiting either dull or non-dull appearing skin. Histological assessment of glycation was performed for representative subjects among the 20-29 years sub-group by immunofluorescence staining of AGEs. LC-MS methods and keratinocyte cell culture were used to assess impact of autophagy modulators and skin care materials on carboxymethyl lysine (CML) amount, a representative AGE. Notable amounts of AGEs were observed in the epidermal samples among young females. Interestingly, the amount of AGEs was significantly higher among the dull skin appearance group. Treatment of keratinocytes with glyceraldehyde (GLA) enhanced CML in the cells, and postglycation treatment with autophagy activators reduced CML. Two skin care materials, Nymphaea alba flower extract (a.k.a. white water lily extract) and sucrose dilaurate, were identified based from in vitro autophagy activation and found to reduce CML in keratinocytes. We found AGEs accumulate in the facial epidermis even among young people, correlating to a yellow and dull appearance. We also demonstrated in vitro activation of autophagy can reduce AGEs in keratinocytes, and autophagy activating skin care materials, N. alba flower extract and sucrose dilaurate, also reduce AGEs in the keratinocyte in vitro model. These data suggest epidermal AGEs contribute to the dull skin appearance, and autophagy activators may provide an effective solution to improve dull appearance by removing and recycling the accumulated glycation in the skin.
Sections du résumé
BACKGROUND
BACKGROUND
The accumulation of advanced glycation end products (AGEs) can impact cellular homoeostasis and protein structure, thus is implicated in numerous skin conditions including yellow, dull appearance. AGE formation is irreversible; thus, understanding of the recycling process of AGEs in the skin is critical for addressing skin appearance conditions.
OBJECTIVE
OBJECTIVE
To determine whether (i) accumulation of AGEs occurs in dull appearance group among young population (age 20-29) (ii) in vitro autophagy stimulation results in reduction of AGEs in keratinocytes.
METHODS
METHODS
Facial cheek biopsies were collected from Chinese women (age 20-50) exhibiting either dull or non-dull appearing skin. Histological assessment of glycation was performed for representative subjects among the 20-29 years sub-group by immunofluorescence staining of AGEs. LC-MS methods and keratinocyte cell culture were used to assess impact of autophagy modulators and skin care materials on carboxymethyl lysine (CML) amount, a representative AGE.
RESULTS
RESULTS
Notable amounts of AGEs were observed in the epidermal samples among young females. Interestingly, the amount of AGEs was significantly higher among the dull skin appearance group. Treatment of keratinocytes with glyceraldehyde (GLA) enhanced CML in the cells, and postglycation treatment with autophagy activators reduced CML. Two skin care materials, Nymphaea alba flower extract (a.k.a. white water lily extract) and sucrose dilaurate, were identified based from in vitro autophagy activation and found to reduce CML in keratinocytes.
CONCLUSION
CONCLUSIONS
We found AGEs accumulate in the facial epidermis even among young people, correlating to a yellow and dull appearance. We also demonstrated in vitro activation of autophagy can reduce AGEs in keratinocytes, and autophagy activating skin care materials, N. alba flower extract and sucrose dilaurate, also reduce AGEs in the keratinocyte in vitro model. These data suggest epidermal AGEs contribute to the dull skin appearance, and autophagy activators may provide an effective solution to improve dull appearance by removing and recycling the accumulated glycation in the skin.
Substances chimiques
Glycation End Products, Advanced
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
12-18Subventions
Organisme : The Procter & Gamble Company
Informations de copyright
© 2020 European Academy of Dermatology and Venereology.
Références
Sell DR, Biemel KM, Reihl O, Lederer MO, Strauch CM, Monnier VM. Glucosepane is a major protein cross-link of the senescent human extracellular matrix: relationship with diabetes. J Biol Chem 2005; 280: 12310-12315.
Gkogkolou P, Böhm M. Advanced glycation end products: key players in skin aging? Dermato-Endocrinology 2012; 4: 259-270.
Crisan M, Taulescu M, Crisan D et al. Expression of advanced glycation end-products on sun-exposed and non-exposed cutaneous sites during the ageing process in humans. PLoS ONE 2013; 8: e75003.
Ho TT, Warr MR, Adelman ER et al. Autophagy maintains the metabolism and function of young and old stem cells. Nature 2017; 543: 205-210.
Kawabata K, Yoshikawa H, Saruwatari K et al. The presence of N-(carboxymethyl)lysine in the human epidermis. Biochem Biophys Acta 2011; 1814: 1246-1252.
Luo W, Friedman MS, Shedden K, Hankenson KD, Woolf PJ. GAGE: generally applicable gene set enrichment for pathway analysis. BMC Bioinformatics 2009; 10: 161.
Kim Y, Guan KL. mTOR: a pharmacologic target for autophagy regulation. J Clin Invest 2015; 125: 25-32.
Koukourakis MI, Giatromanolaki A, Fylaktakidou K et al. SMER28 is a mTOR-independent small molecule enhancer of autophagy that protects mouse bone marrow and liver against radiotherapy. Invest New Drugs 2018; 36: 773-781.
Shin ES, Sang PY, Nam SH. Non-invasive assessments of the advanced glycation end products in human skin using reflectance NIR spectroscopy. IEEE Eng Med Biol Soc 2019; 2019: 5506-5509.
Iannuzzi C, Irace G, Sirangelo I. Differential effects of glycation on protein aggregation and amyloid formation. Front Mol Biosci 2014; 1: 9.
Nahomi RB, Oya-Ito T Nagaraj RH. The combined effect of acetylation and glycation on the chaperone and anti-apoptotic functions of human α-crystallin. Biochim Biophys Acta 2013; 1832: 195-203.
Semenyuk P, Barinova K, Muronetz V. Glycation of α-synuclein amplifies the binding with glyceraldehyde-3-phosphate dehydrogenase. Int J Biol Macromol 2019; 127: 278-285.
Zheng Q, Omans ND, Leicher R et al. Reversible histone glycation is associated with disease-related changes in chromatin architecture. Nat Commun 2019; 10: 1289.
Takahashi A, Takabatake Y, Kimura T et al. Autophagy inhibits the accumulation of advanced glycation end products by promoting lysosomal biogenesis and function in the kidney proximal tubules. Diabetes 2017; 66: 1359-1372.
Hu P, Zhou H, Lu M et al. Autophagy plays a protective role in advanced glycation end product-induced apoptosis in cardiomyocytes. Cell Physiol Biochem 2015; 37: 697-706.