Biologic Characteristics of Cultured Human Vitiligo Melanocytes

Im, Sang Hee; Hann, Seung Kyung; Kim, Hyung Il; Kim, Nam Soo; Park, Yoon‐Kee

doi:10.1111/j.1365-4362.1994.tb02895.x

Cited by 29 publications

(22 citation statements)

References 21 publications

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“…We hypothesized that oxidative stress in melanocytes leads to disruption of the folding machinery of the ER, which is dependent upon redox reactions for formation of disulphide bonds. In support of this idea is ER dilation in melanocytes at the periphery of vitiligo lesions and in melanocytes cultured from vitiligo patients (Boissy et al , 1991; Im et al , 1994; Le Poole et al , 2000). Accumulation of immature proteins in the ER results in activation of the UPR, a pathway also implicated in determining susceptibility to vitiligo in genetic association studies linking an XBP1 polymorphism with increased risk of developing the disorder (Ren et al , 2009).…”

Section: Discussionmentioning

confidence: 74%

Vitiligo-Inducing Phenols Activate the Unfolded Protein Response in Melanocytes Resulting in Upregulation of IL6 and IL8

Toosi

Orlow

Manga

2012

Journal of Investigative Dermatology

163

138

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Vitiligo is characterized by depigmented skin patches due to loss of epidermal melanocytes. Oxidative stress may play a role in vitiligo onset, while autoimmunity contributes to disease progression. In this study we sought to identify mechanisms that link disease triggers and spreading of lesions. A hallmark of melanocytes at the periphery of vitiligo lesions is dilation of the endoplasmic reticulum (ER). We hypothesized that oxidative stress results in redox disruptions that extend to the ER, causing accumulation of misfolded peptides, which activates the unfolded protein response (UPR). We used 4-tertiary butyl phenol (4-TBP) and monobenzyl ether of hydroquinone (MBEH), known triggers of vitiligo. We show that expression of key UPR components, including the transcription factor X-box binding protein 1 (XBP1), are increased following exposure of melanocytes to phenols. XBP1 activation increases production of immune mediators interleukin-6 (IL6) and IL8. Co-treatment with XBP1 inhibitors reduced IL6 and IL8 production induced by phenols, while over-expression of XBP1 alone increased their expression. Thus, melanocytes themselves produce cytokines associated with activation of an immune response following exposure to chemical triggers of vitiligo. These results expand our understanding of the mechanisms underlying melanocyte loss in vitiligo and pathways linking environmental stressors and autoimmunity.

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Section: Discussionmentioning

confidence: 74%

Vitiligo-Inducing Phenols Activate the Unfolded Protein Response in Melanocytes Resulting in Upregulation of IL6 and IL8

Toosi

Orlow

Manga

2012

Journal of Investigative Dermatology

163

138

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“…Melanocyte abnormality and destruction, melanin-concentrating hormone (MCH) MCH receptor autoantibodies, the overexpression of MCH, a high level of homocysteine, an increase in catecholamine, free oxygen radicals, cytomegalovirus and stress may be related to the pathogenesis of vitiligo (14,15,16,17,18,19). MetS (insulin resistance syndrome or syndrome X) generally includes abdominal obesity, hyperglycaemia, dyslipidaemia and hypertension (20), and several definitions of MetS have been described by different organisations.…”

Section: Discussionmentioning

confidence: 99%

Increased Risk of Metabolic Syndrome in Patients with Vitiligo

Ataş

Gönül

2017

Balkan Med J

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Background:Inflammatory and immune processes can be triggered in vitiligo due to a decreased number of melanocytes and their anti-inflammatory effects. Because of the systemic nature of vitiligo, metabolic abnormalities such as insulin resistance and lipid profile disturbances as well as skin involvement may be observed in vitiligo.Aims:To investigate the association between metabolic syndrome and vitiligo.Study Design:Case-control study.Methods:The demographic, clinical and laboratory features in the subjects were compared according to presence of vitiligo and metabolic syndrome [patients (n=63) vs. gender-age matched controls (n=65) and metabolic syndrome positive (n=38) vs. negative (n=90)]. A logistic regression analysis was also used.Results:We identified metabolic syndrome in 24 (38.1%) subjects with vitiligo and 14 (21.5%) subjects without vitiligo (p=0.04). Active vitiligo, segmental vitiligo, an increased duration of vitiligo and an increased percentage in the affected body surface area were determined to be independent predictors of metabolic syndrome [activity of vitiligo: p=0.012, OR (95% CI)=64.4 (2.5-1672); type of vitiligo: p=0.007, OR (95% CI)=215.1 (4.3-10725.8); duration of vitiligo: p=0.03, OR (95% CI)=1.4 (1.1-2.0); percentage of affected body surface area: p=0.07, OR (95% CI)=1.2 (0.98-1.5)].Conclusion:The risk of developing metabolic syndrome is increased in patients with vitiligo. The poor clinical features of vitiligo, such as active, extended and segmental vitiligo with an increased duration of time, are independent predictors for developing metabolic syndrome.

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“…Vitiligo melanocytes are known to have intrinsic defects, which limit their stability and survival and subsequently lead to depigmentation . Differential characterization and mosaicism of body melanocytes were described in nonsegmental vitiligo, as identified in segmental cases, harboring fragile melanocyte populations, which are susceptible to external as well as auto‐inflammatory mechanisms .…”

Section: Discussionmentioning

confidence: 99%