Secreted Frizzled-Related Protein 2 (sFRP2) Functions as a Melanogenic Stimulator; the Role of sFRP2 in UV-Induced Hyperpigmentary Disorders

Kim, Mi-Sun; Han, Jae Ho; Kim, Jang-Hee; Park, Tae Jun; Kang, Hee Young

doi:10.1038/jid.2015.365

Cited by 56 publications

(56 citation statements)

References 39 publications

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“…A transcriptional analysis performed in melasma lesions compared to surrounding healthy skin then clearly emphasized the complexity of this disorder by revealing almost 300 genes to be significantly differentially regulated, affecting not only melanocytes but also the dermis component . These results further demonstrate that fibroblast-secreted factors, such as WIF1 (Kim, Lee, & Lee, 2013) or sFRP2 (Kim, Han, Kim, Park, & Kang, 2016), are involved in the pathophysiology of melasma. These data are in line with the reports that fibroblasts isolated from photoaging skin produce a greater amount of promelanogenic growth factors, such as KGF, HGF, and SCF, and that the in vitro photo-induced senescencelike phenotype of fibroblasts leads to the increased production of the same factors (Briganti et al, 2013).…”

Section: Introductionsupporting

confidence: 59%

Melasma, a photoaging disorder

Passeron

Picardo

2018

Pigment Cell Melanoma Res

186

194

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Summary Melasma is a common hyperpigmentary disorder. The impact on the quality of life of affected individuals is well demonstrated, demanding new therapeutic strategies. However, the treatment of melasma remains highly challenging. Melasma is often considered as the main consequence of female hormone stimulation on a predisposed genetic background. Although these two factors do contribute to this acquired pigmentary disorder, the last decade has revealed several other key players and brought new pieces to the complex puzzle of the pathophysiology of melasma. Here, we summarize the latest evidence on the pathophysiology of melasma, and we suggest that melasma might be a photoaging skin disorder affecting genetically predisposed individuals. Such data must be taken into consideration by clinicians as they could have a profound impact on the treatment and the prevention of melasma.

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Section: Introductionsupporting

confidence: 59%

Melasma, a photoaging disorder

Passeron

Picardo

2018

Pigment Cell Melanoma Res

186

194

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“…However, positive effects of sFRPs in Wnt signalling have been discovered via stimulation of the β‐catenin pathway . Among skin cells, fibroblasts highly express sFRP2, and the secretion level is significantly upregulated in the hyperpigmentary skin lesions of solar lentigo and melasma and in acutely UV‐irradiated skin . sFRP2 increases melanogenesis in normal human fibroblast–melanocyte cocultures through activation of the β‐catenin–MITF–tyrosinase pathway, showing it to be an effective mesenchymal melanogenic inducer …”

Section: Fibroblastsmentioning

confidence: 99%

“…66 sFRP2 increases melanogenesis in normal human fibroblast-melanocyte cocultures through activation of the b-catenin-MITF-tyrosinase pathway, showing it to be an effective mesenchymal melanogenic inducer. 66 Wnt inhibitory factor (WIF)-1, which is also an important secreted antagonist of Wnt signalling, has been shown to be expressed in human fibroblasts and keratinocytes. A recent study using microarray analysis has indicated that WIF-1 gene expression is significantly reduced in hyperpigmented skin compared with normally pigmented skin in patients with melasma.…”

Section: Scf Edn1mentioning

confidence: 99%

Paracrine regulation of melanogenesis

Yuan

Jin

2018

Br J Dermatol

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Melanocytes are generally characterized by the basic ability of melanin synthesis and transfer to adjacent keratinocytes. This constitutes an individual skin phenotype and provides epidermal protection from various stimuli, such as ultraviolet irradiation, through a complex process called melanogenesis, which can be regulated by autocrine or paracrine factors. Recent evidence has revealed the paracrine effects of keratinocytes on melanogenesis by secreting cytokines, including α-melanocyte stimulating hormone and endothelin-1. In addition to keratinocytes, there are other types of cells in the skin, such as fibroblasts and immune cells, which are also actively involved in the regulation of melanocyte behaviour through the production of paracrine factors. In addition, extracellular matrix proteins, which are secreted mainly by skin-resident cells, not only play direct roles in regulating melanocyte morphology and functions but also provide structural support between the epidermis and dermis to control the distribution of various secreted cytokines from keratinocytes and/or fibroblasts, which are potentially involved in the regulation of melanogenesis. Moreover, understanding the origin of melanocytes (neural crest cells) and the presence of nerve endings in the epidermis can reveal the intimate contact between melanocytes and cutaneous specific nervous system proteins. Melanocytes are associated with all these networks with corresponding receptors expressed on the cell surface. In this review, we provide an overview of recent advances in determining the intimate relationships between melanocytes and their surrounding elements, which provide insights into the complex nature of the regulation of melanogenesis.

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“…Early studies found that sFRP binding to Wnt prevented the activation of Wnt receptors, leading to the initial classification of sFRPs as Wnt signaling inhibitors [27,28]. However, subsequent finding has suggested that sFRP2 functions as a melanogenic stimulator through Wnt/b-catenin signaling, but the precise mechanism needs to be clarified [29]. Kim et al highlighted a certain paracrine role of fibroblast-derived sFRP2 in pigmentation.…”

Section: Sfrpmentioning

confidence: 99%