4-Tertiary Butyl Phenol Exposure Sensitizes Human Melanocytes to Dendritic Cell-Mediated Killing: Relevance to Vitiligo

Kroll, Tara M.; Bommiasamy, Hemamalini; Boissy, Raymond E.; Hernandez, Claudia; Nickoloff, Brian J.; Mestril, Ruben; Poole, I. Caroline Le

doi:10.1111/j.0022-202x.2005.23653.x

Cited by 150 publications

(132 citation statements)

References 32 publications

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“…HSPA may also play a role in the development of vitiligo, a T-cell mediated autoimmune disease characterized by skin depigmentation. HSPA was shown to be released by stressed melanocytes in culture, which may mediate DC activation that led to killing of stressed melanocytes (Kroll et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Heat treatment increases the incidence of alopecia areata in the C3H/HeJ mouse model

Wikramanayake¹,

Alvarez‐Connelly²,

Simon³

et al. 2010

Cell Stress and Chaperones

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Alopecia areata (AA) is a common autoimmune disease characterized by non-scarring hair loss. Previous studies have demonstrated an association between AA and physiological/psychological stress. In this study, we investigated the effects of heat treatment, a physiological stress, on AA development in C3H/HeJ mice. Whereas this strain of mice are predisposed to AA at low incidence by 18 months of age, we observed a significant increase in the incidence of hair loss in heat-treated 8-month-old C3H/HeJ mice compared with sham-treated mice. Histological analysis detected mononuclear cell infiltration in anagen hair follicles, a characteristic of AA, in heat-treated mouse skin. As expected, increased expression of induced HSPA1A/B (formerly called HSP70i) was detected in skin samples from heat-treated mice. Importantly, increased HSPA1A/B expression was also detected in skin samples from C3H/HeJ mice that developed AA spontaneously. Our results suggest that induction of HSPA1A/B may precipitate the development of AA in C3H/HeJ mice. For future studies, the C3H/HeJ mice with heat treatment may prove a useful model to investigate stress response in AA.

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Section: Discussionmentioning

confidence: 99%

Heat treatment increases the incidence of alopecia areata in the C3H/HeJ mouse model

Wikramanayake¹,

Alvarez‐Connelly²,

Simon³

et al. 2010

Cell Stress and Chaperones

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show abstract

“…The mechanism involves specific dendritic/T-cell activation and melanocyte recognition. The latter can also be triggered by treatment with chemical sensitizers: 4-tertiary butyl phenol (Kroll et al, 2005) and triglycidyl-p-aminophenol (Jappe et al, 2005) seem to be candidates.…”

Section: Melanocyte Lossmentioning

confidence: 99%

Hypopigmenting agents: an updated review on biological, chemical and clinical aspects

Solano¹,

Briganti²,

Picardo³

et al. 2006

Pigment Cell Research

611

521

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SummaryAn overview of agents causing hypopigmentation in human skin is presented. The review is organized to put forward groups of biological and chemical agents. Their mechanisms of action cover (i) tyrosinase inhibition, maturation and enhancement of its degradation; (ii) Mitf inhibition; (iii) downregulation of MC1R activity; (iv) interference with melanosome maturation and transfer; (v) melanocyte loss, desquamation and chemical peeling. Tyrosinase inhibition is the most common approach to achieve skin hypopigmentation as this enzyme catalyses the rate-limiting step of pigmentation. Despite the large number of tyrosinase inhibitors in vitro, only a few are able to induce effects in clinical trials. The gap between in-vitro and in-vivo studies suggests that innovative strategies are needed for validating their efficacy and safety. Successful treatments need the combination of two or more agents acting on different mechanisms to achieve a synergistic effect. In addition to tyrosinase inhibition, other parameters related to cytotoxicity, solubility, cutaneous absorption, penetration and stability of the agents should be considered. The screening test system is also very important as keratinocytes play an active role in modulating melanogenesis within melanocytes. Mammalian skin or at least keratinocytes/melanocytes co-cultures should be preferred rather than pure melanocyte cultures or soluble tyrosinase.

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“…The major stress-induced member of the Hsp family, Hsp70 (also called Hsp72), has been reported to effectively rescue various cell types from apoptosis when exposed to heat shock, tumor necrosis factor-a (TNF-a), oxidative stress, irradiation or anti-cancer drugs (12). On the other hand, adenoviral overexpression of Hsp70 in Mc0009 P12 melanocytes did not protect against 4-tertiary butyl phenol induced apoptosis (13).…”

Section: Introductionmentioning

confidence: 99%

Hsp70 protects against UVB induced apoptosis by preventing release of cathepsins and cytochrome c in human melanocytes

2006

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Stress-induced heat shock protein 70 (Hsp70) effectively protects cells against apoptosis, although the anti-apoptotic mechanism is still undefined. Exposure of human melanocytes to heat and subsequent UVB irradiation increased the level of Hsp70 and pre-heating reduced UVB induced apoptosis. Immunofluorescence staining of Hsp70 in combination with staining of lysosomes (Lamp2) or mitochondria (Mitotracker Ò ) in pre-heated UVB exposed cells showed co-localization of Hsp70 with both lysosomes and mitochondria in the surviving cell population. Furthermore, UVB induced apoptosis was accompanied by lysosomal and mitochondrial membrane permeabilization, detected as release of cathepsin D and cytochrome c, respectively, which were prevented by heat pre-treatment. In purified fractions of lysosomes and mitochondria, recombinant Hsp70 attached to both lysosomal and mitochondrial membranes. Moreover, in apoptotic cells Bax was translocated from a diffuse cytosolic location into punctate mitochondrial-like structures, which was inhibited by Hsp70 induction. Such inhibition of Bax translocation was abolished by transfection with Hsp70 siRNA. Furthermore, Hsp70 siRNA eliminated the apoptosis preventive effect observed after pre-heating. These findings show Hsp70 to rescue melanocytes from UVB induced apoptosis by preventing release of cathepsins from lysosomes, Bax translocation and cytochrome c release from mitochondria.

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4-Tertiary Butyl Phenol Exposure Sensitizes Human Melanocytes to Dendritic Cell-Mediated Killing: Relevance to Vitiligo

Cited by 150 publications

References 32 publications

Heat treatment increases the incidence of alopecia areata in the C3H/HeJ mouse model

Heat treatment increases the incidence of alopecia areata in the C3H/HeJ mouse model

Hypopigmenting agents: an updated review on biological, chemical and clinical aspects

Hsp70 protects against UVB induced apoptosis by preventing release of cathepsins and cytochrome c in human melanocytes

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