TRP-2 expression protects HEK cells from dopamine- and hydroquinone-induced toxicity

Michard, Quentin; Commo, S; Rocchetti, Jill; Houari, F. El; Alleaume, Anne-Marie; Wakamatsu, Kazumasa; Ito, Shosuke; Bernard, Bruno

doi:10.1016/j.freeradbiomed.2008.06.030

Cited by 20 publications

(12 citation statements)

References 35 publications

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“…These effects were reversed with TRP-2 silencing, confirming the antioxidative activity of TRP-2 [86]. Later studies of epidermal keratinocytes documented a more specific role for TRP-2 in protecting from reactive quinone metabolites (dopamine and hydroquinone), but not from DOPAchrome [87]. The antioxidant role of TRP-2 and its possible depletion from pigmented bulbar melanocytes, but not from eyelash melanocytes [82,84], might suggest another antioxidant pathway that could affect hair greying.…”

Section: Trp-2 and Hair Pigmentationmentioning

confidence: 76%

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

Seiberg¹

2013

Intern J of Cosmetic Sci

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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...

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Section: Trp-2 and Hair Pigmentationmentioning

confidence: 76%

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

Seiberg¹

2013

Intern J of Cosmetic Sci

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“…S1). Previous studies have indicated a role for this gene product in pigment development and the modulation of cell responses to oxidative stress (31,32). In Figure 9A, we used a lentivirus system to deliver specific shRNA to reduce DCT levels (clone 38) by ≈75% in hfRPE.…”

Section: Resultsmentioning

confidence: 99%

Transcriptome analysis and molecular signature of human retinal pigment epithelium

Strunnikova

Maminishkis

Barb

et al. 2010

Human Molecular Genetics

230

227

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Retinal pigment epithelium (RPE) is a polarized cell layer critical for photoreceptor function and survival. The unique physiology and relationship to the photoreceptors make the RPE a critical determinant of human vision. Therefore, we performed a global expression profiling of native and cultured human fetal and adult RPE and determined a set of highly expressed ‘signature’ genes by comparing the observed RPE gene profiles to the Novartis expression database (SymAtlas: ) of 78 tissues. Using stringent selection criteria of at least 10-fold higher expression in three distinct preparations, we identified 154 RPE signature genes, which were validated by qRT-PCR analysis in RPE and in an independent set of 11 tissues. Several of the highly expressed signature genes encode proteins involved in visual cycle, melanogenesis and cell adhesion and Gene ontology analysis enabled the assignment of RPE signature genes to epithelial channels and transporters (ClCN4, BEST1, SLCA20) or matrix remodeling (TIMP3, COL8A2). Fifteen RPE signature genes were associated with known ophthalmic diseases, and 25 others were mapped to regions of disease loci. An evaluation of the RPE signature genes in a recently completed AMD genomewide association (GWA) data set revealed that TIMP3, GRAMD3, PITPNA and CHRNA3 signature genes may have potential roles in AMD pathogenesis and deserve further examination. We propose that RPE signature genes are excellent candidates for retinal diseases and for physiological investigations (e.g. dopachrome tautomerase in melanogenesis). The RPE signature gene set should allow the validation of RPE-like cells derived from human embryonic or induced pluripotent stem cells for cell-based therapies of degenerative retinal diseases.

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“…Recent data from our laboratory have shown that dopachrome tautomerase levels may be associated with protection against oxidative stress in EMs (Gledhill et al, unpublished). Dopachrome tautomerase may also provide such protection from quinone metabolites (Michard et al, 2008), highlighting an additional non-pigmentary role for this enzyme in maintaining cellular redox status. The precise relationship between dopachrome tautomerase and eumelanogenic HFMs remains unresolved, as this relationship seems to vary between follicles from different body sites (Commo et al, 2004;Thibaut et al, 2009).…”

mentioning

confidence: 99%

Human Hair Follicle and Epidermal Melanocytes Exhibit Striking Differences in Their Aging Profile which Involves Catalase

Kauser

Westgate

Green

et al. 2011

Journal of Investigative Dermatology

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still whereas others actively migrated in the DNFB-applied skin. We assume that this distinct migratory activity may be due to the fact that not all T cells in the LNs after DNFB sensitization were DNFB specific. In contrast, almost all TNCB-sensitized T cells actively migrated when DNFB was applied. In addition, we showed reverse motile activities in the TNCB-painted skin. Moreover, skin-infiltrating T cells colocalized with APCs. These findings suggest that skin-infiltrating T cells may actively scan for antigens, and when they meet APCs carrying their specific antigens, they stop migrating and stably interact with APCs. Our results also indicate that in the elicitation phase of CHS, hapten seems to be presented mainly by APCs in the dermis. Additional detailed studies are needed to clarify which subset of dermal APCs is essential for hapten presentation and whether epidermal Langerhans cells contribute.

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TRP-2 expression protects HEK cells from dopamine- and hydroquinone-induced toxicity

Cited by 20 publications

References 35 publications

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

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

Transcriptome analysis and molecular signature of human retinal pigment epithelium

Human Hair Follicle and Epidermal Melanocytes Exhibit Striking Differences in Their Aging Profile which Involves Catalase

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