Age‐induced hair greying – the multiple effects of oxidative stress

Abstract

SynopsisAn obvious sign of ageing is hair greying, or the loss of pigment production and deposition within the hair shafts. Numerous mechanisms, acting at different levels and follicular locations, contribute to hair greying, ranging from melanocyte stem cells defects to follicular melanocyte death. One key issue that is in common to these processes is oxidative damage. At the hair follicle stem cells niche, oxidative stress, accelerated by B-cell lymphoma 2 gene (BCL-2) depletion, leads to selective apoptosis and diminution of melanocyte stem cells, reducing the repopulation of newly formed anagen follicles. Melanotic bulbar melanocytes express high levels of BCL-2 to enable survival from melanogenesis-and ultraviolet A (UVA)-induced reactive oxygen species (ROS) attacks. With ageing, the bulbar melanocyte expression of anti-oxidant proteins such as BCL-2, and possibly TRP-2, is reduced, and the dedicated enzymatic anti-oxidant defence system throughout the follicle weakens, resulting in enhanced oxidative stress. A marked reduction in catalase expression and activity results in millimolar accumulation of hydrogen peroxide, contributing to bulbar melanocyte malfunction and death. Interestingly, amelanotic melanocytes at the outer root sheath (ORS) are somewhat less affected by these processes and survive for longer time even within the white, ageing hair follicles. Better understanding of the overtime susceptibility of melanocytes to oxidative stress at the different follicular locations might yield clues to possible therapies for the prevention and reversal of hair greying.R esum e Un signe evident du vieillissement est le grisonnement des cheveux ou la perte de la production de pigment et de son d epôt dans les follicules pileux. De nombreux m ecanismes, agissant a diff erents niveaux et endroits folliculaires, contribuent aux cheveux grisonnants, allant des dommages aux cellules souches m elanocytaires a la mort des m elanocytes folliculaires. Une question cl e qui est commune a ces processus concerne le dommage oxydatif. Au niveau de la niche des cellules souches du follicule, le stress oxydatif, acc el er e par l'appauvrissement de BCL-2, conduit a l'apoptose et a une diminution s elective des cellules souches des m elanocytes, ce qui r eduit le repeuplement des follicules anag enes nouvellement form es. Les m elanocytes bulbaires m elaniques expriment des niveaux elev es de Bcl-2 pour permettre la survie suite a l'attaque par les esp eces r eactives de l'oxyg ene (ROS) induites par la m elanog en ese et les ultraviolets A (UVA). Avec le vieillissement, l'expression dans m elanocytes du bulbe des prot eines anti-oxydantes comme BCL-2, et peut-être TRP-2, est r eduite, et la d efense sp ecifique du syst eme antioxydant enzymatique faiblit a travers le follicule, r esultant en un plus grand stress oxydatif. Une r eduction marqu ee de l'expression catalase et les r esultats de l'activit e de l'accumulation millimolaire de peroxyde d'hydrog ene contribuent a un dysfonctionnement et a la mort des m elanocytes b...

Programmed cell death in aging

“…Age-related hearing loss involves loss of sensory hair cells via PCD, and mitochondrial genome mutations are implicated in this process(Fujimoto and Yamasoba, 2014). Aging-associated hair greying involves loss of melanocyte stem cells by PCD, and decreased Bcl-2 and increased ROS are implicated in this process (Seiberg, 2013). Finally, increased sensitivity to stress and PCD is observed in aging gastric mucosa, and rodent studies implicate caspase-3 activation (Tarnawski et al, 2014).…”

Improvement of Hair Graying during a Treatment of Male Pattern Hair Loss Using 1,927-nm Fractionated Thulium Laser Energy and Polydeoxyribonucleotide Injections

“…Various mechanisms were suggested for hair graying, such as melanocyte stem cells depletion, melanocyte migration defects, anagen defects, melanocyte apoptosis, and pigmentary machinery defects, all of which have been found to be related to oxidative stress. 5 Melanocyte stem cells in hair are vulnerable to oxidative damage. Upon continued oxidative stress, melanocyte stem cells eventually fail to repopulate themselves, which leads to hair matrix melanocyte depletion and hair graying.…”

“…Upon continued oxidative stress, melanocyte stem cells eventually fail to repopulate themselves, which leads to hair matrix melanocyte depletion and hair graying. 5,6 The B-cell lymphoma 2 gene (BCL-2) is an anti-apoptotic oncogene that inhibits cell death, particularly in microenvironments with oxidative stress. 7 As BCL-2 expression declines in aged hair follicles, melanocyte stem cells become more susceptible to oxidative stress, because of decreased protective effect from BCL-2.…”

“…7 As BCL-2 expression declines in aged hair follicles, melanocyte stem cells become more susceptible to oxidative stress, because of decreased protective effect from BCL-2. 5 Though the mechanisms of hair graying are widely studied and hair graying is a major concern for aged people, there is currently no therapeutic method proven to prevent or reverse hair graying. Hair dyes and coloring are the most common way to reverse hair graying currently.…”

Biology of the eyelash hair follicle: an enigma in plain sight

“…78,[83][84][85][86] Taking into account that (i) in most individuals, ELs retain their pigment considerably longer than in human scalp, beard or body hair; 87 (ii) the rapid cyclic regeneration of the HF pigmentary unit requires a highly functional reservoir of HF melanocyte stem cells; 78 epithelial stem cells, [88][89][90] ELHFs must contain a pool of melanocyte and epithelial HF stem cells.…”