Gene Expression Profiling in Melasma in Korean Women

Chung, Bo Young; Noh, Tai Kyung; Yang, Soo Jung; Kim, Il Hwan; Lee, Mi Woo; Yoon, Tae Jin; Chang, Sung Eun

doi:10.1159/000365080

Cited by 23 publications

(25 citation statements)

References 61 publications

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“…Consistent with our previous microarray data (Chung et al., ), quantitative reverse transcription PCR (qRT‐PCR) confirmed that adiponectin mRNA and protein level were lower in the lesional skin of melasma patients compared with non‐lesional skin (Figure a). Interestingly, while the expression of cytokeratin and melan‐A appears to be comparable, by IF staining, we observed decreased AdipoR1 and AdipoR2 expression in the basal layer of lesional skin compared with non‐lesional skin of melasma patients (Figures b, Fig ).…”

supporting

confidence: 90%

“…Interestingly, our previous work has shown that using cDNA analysis of melasma skin biopsy specimens from five Korean women, adiponectin mRNA expression was significantly decreased in the lesional skin in comparison with the non‐lesional skin (Chung et al., ). Hence, in this study, we pursue the role of adiponectin and another well‐known AMPK activator, AICAR on melanogenesis and speculate clinical relevance of adiponectin in melasma, a common but refractory hyperpigmentary skin disorder.…”

mentioning

confidence: 99%

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Novel regulation of melanogenesis by adiponectin via the AMPK/CRTC pathway

Bang

Won

Moon

et al. 2017

Pigment Cell Melanoma Res

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Several studies observed that adiponectin, an important adipokine that improves glucose metabolism by regulating AMP-activated protein kinase (AMPK) signaling, is dermatologically beneficial. In our recent microarray data, we found that adiponectin expression was lower in lesional skin than in non-lesional skin of melasma patients. Given that AMPK is a key adiponectin signaling mediator, we investigated the role of adiponectin and AICAR, a cell-permeable AMPK activator, in melanogenesis. We herein showed that adiponectin and AICAR downregulated MITF, tyrosinase, TRP-1, and DCT expression and reduced melanin content in normal human and mouse melanocytes. The depigmenting effect of adiponectin was mediated via AMPK activation, which induced the inhibitory phosphorylation of CREB-regulated transcription co-activators (CRTCs) and subsequent suppression of the novel CRTC/CREB pathway in melanocytes. These findings suggest that adiponectin and its analogs are useful as a clinical strategy for treating hyperpigmentation disorders.

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supporting

confidence: 90%

mentioning

confidence: 99%

Novel regulation of melanogenesis by adiponectin via the AMPK/CRTC pathway

Bang

Won

Moon

et al. 2017

Pigment Cell Melanoma Res

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“…In our previous study using DNA microarray from melasma lesions, GDA was shown to be one of the most upregulated genes, which was validated by qRT-PCR analysis [17]. KCs were the most abundant type of cells obtained from a skin biopsy using a 2 mm punch, and high GDA expression in cultured KCs suggested that KCs are the source of GDA in hyperpigmented lesions.…”

Section: Discussionmentioning

confidence: 67%

“…Similar to melasma, Riehl's melanosis (RM) is characterized by diffuse hyperpigmentary patches on the face and neck and is aggravated by UV irradiation and/or inflammation [15,16]. In our previous study, we found that guanine deaminase (GDA) mRNA expression was 5 to 14-fold higher in melasma lesion tissue than in non-lesion tissue [17]. In purine metabolism, guanine is converted into xanthine by GDA, a ubiquitous aminohydrolase enzyme.…”

Section: Introductionmentioning

confidence: 99%

Guanine Deaminase in Human Epidermal Keratinocytes Contributes to Skin Pigmentation

Jung

Noh

et al. 2020

Molecules

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Epidermal keratinocytes are considered as the most important neighboring cells that modify melanogenesis. Our previous study used microarray to show that guanine deaminase (GDA) gene expression is highly increased in melasma lesions. Hence, we investigated the role of GDA in skin pigmentation. We examined GDA expression in post-inflammatory hyperpigmentation (PIH) lesions, diagnosed as Riehl’s melanosis. We further investigated the possible role of keratinocyte-derived GDA in melanogenesis by quantitative PCR, immunofluorescence staining, small interfering RNA-based GDA knockdown, and adenovirus-mediated GDA overexpression. We found higher GDA positivity in the hyperpigmentary lesional epidermis than in the perilesional epidermis. Both UVB irradiation and stem cell factor (SCF) plus endothelin-1 (ET-1) were used, which are well-known melanogenic stimuli upregulating GDA expression in both keratinocyte culture alone and keratinocyte and melanocyte coculture. GDA knockdown downregulated melanin content, while GDA overexpression promoted melanogenesis in the coculture. When melanocytes were treated with UVB-exposed keratinocyte-conditioned media, the melanin content was increased. Also, GDA knockdown lowered SCF and ET-1 expression levels in keratinocytes. GDA in epidermal keratinocytes may promote melanogenesis by upregulating SCF and ET-1, suggesting its role in skin hyperpigmentary disorders.

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“…5 Recent studies indicate that several proteins and cellular components, including α-melanocyte-stimulating hormone, stem cell factors, ckit, vascular endothelial growth factor, and nerve growth factor, are involved in the pathogenesis of melasma. 7 Topical agents such as hydroquinone and superficial chemical peels are the current standard for melasma treatment, but concern about side effects and long-term safety has spurred efforts to develop alternative treatment options. 8 Oral intake or intralesional injection of ascorbic acid or tranexamic acid has been clinically tried.…”

Section: Introductionmentioning

confidence: 99%