Factors secreted by irradiated aged fibroblasts induce solar lentigo in pigmented reconstructed epidermis

Salducci, Marine; André, Nathalie; Guéré, Christelle; Martin, Marion; Fitoussi, R.; Vié, Katell; Cario‐André, Muriel

doi:10.1111/pcmr.12234

Cited by 42 publications

(51 citation statements)

References 10 publications

(12 reference statements)

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“…Certain inflammatory factors such as leukotriene C4 also induce chronic growth stimulation of human adult melanocytes (Medrano et al, 1993). On the other hand, it has been shown that different fibroblast-secreted melanogenic peptides could modulate melanocyte numbers in monolayer cultures (Cario-André et al, 2006;Salducci et al, 2014). In vitro results on monolayers and skin reconstructs, using growth factors and conditioned medium suggested that murine fibroblasts secrete soluble factors that can stimulate normal human melanocytes.…”

Section: Discussionmentioning

confidence: 97%

Clonogenic Cell Subpopulations Maintain Congenital Melanocytic Nevi

Charbel

Fontaine

Kadlub

et al. 2015

Journal of Investigative Dermatology

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Large congenital melanocytic nevi (lCMN) are benign melanocytic tumors associated with an increased risk of melanoma transformation. They result predominantly from a post-zygotic somatic NRAS mutation. These lesions persist and even increase after birth proportionally to the child's growth. Therefore, we asked here whether cells with clonogenic and tumorigenic properties persisted postnatally in lCMN. Subpopulations of lCMN cells expressed stem cell/progenitor lineage markers such as Sox10, Nestin, Oct4, and ABCB5. In vitro, 1 in 250 cells from fresh lCMN formed colonies that could be passaged and harbored the same NRAS mutation as the original nevus. In vivo, lCMN specimens xenografted in immunocompromised mice expanded 4-fold. BrdU(+)-proliferating and label-retaining melanocytes were found within the outgrowth skin tissue of these xenografts, which displayed the same benign nested architecture as the original nevus. lCMN cell suspensions were not able to expand when xenografted alone in Rag 2-/- mice. Conversely, when mixed with keratinocytes, these cells reconstituted the architecture of the human nevus with its characteristic melanocyte layout, lentiginous hyperplasia, and nested architecture. Overall, our data demonstrate that, after birth, certain lCMN cell subtypes still display features such as clonogenic potential and expand into nevus-like structures when cooperating with adjacent keratinocytes.

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Section: Discussionmentioning

confidence: 97%

Clonogenic Cell Subpopulations Maintain Congenital Melanocytic Nevi

Charbel

Fontaine

Kadlub

et al. 2015

Journal of Investigative Dermatology

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“…Other features such as damage to the basal membrane, an increase in blood vessels and in dermal mast cells and lymphohistiocytic infiltration have been described . The aetiology of melasma seems more complex than that of senile lentigo, another photoageing disorder, which can be attributed mainly to dysregulation of UVA‐induced fibroblasts . As summarized by Passeron and Picardo, solar radiation (UVA, UVB and visible light) can induce melanogenesis in melasma by stimulating melanocytes directly or indirectly via secretion of melanogenic factors by keratinocytes, fibroblasts, endothelial cells and probably sebocytes.…”

Section: Hormones and Melasma In Vivomentioning

confidence: 99%

“…First, in melasma, the number of blood vessels and mast cells is greater in lesional skin than in perilesional skin . Second, dermal regulation of pigmentation has already been demonstrated in vitro, [ ] in vivo and in pigmentary disorders such as senile lentigo and vitiligo and has been hypothesized in melasma . Furthermore, in systemic scleroderma (SSc) whose main skin feature is fibrosis, characteristic modifications of the fibroblast functional phenotype are thought to be due to an interplay between damaged endothelial cells, immune cells and their soluble mediators .…”

Section: Effects Of Sex Steroid Hormones On Dermal Compartment and Inmentioning

confidence: 99%

How hormones may modulate human skin pigmentation in melasma: An in vitro perspective

Cario‐André

2019

Experimental Dermatology

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Melasma is a common acquired hyperpigmentary disorder occurring primarily in photo‐exposed areas and mainly affecting women of childbearing age. To decipher the role of sex hormones in melasma, this viewpoint reviews the effects of sex hormones on cutaneous cells cultured in monolayers, in coculture, in 3D models and explants in the presence or the absence of UV. The data show that sex steroid hormones, especially oestrogen, can modulate in vitro pigmentation by stimulating melanocytes and keratinocyte pro‐pigmentary factors, but not via fibroblast or mast cell activation. In vitro data suggest that oestrogen acts on endothelial cell count, which may in turn increase endothelin‐1 concentrations. However, data on explants revealed that sex steroid even at doses observed during pregnancy cannot induce melanogenesis alone nor melanosome transfer but that it acts in synergy with UVB. In conclusion, we hypothesize that in predisposed persons, sex steroid hormones initiate hyperpigmentation in melasma by amplifying the effects of UV on melanogenesis via direct effects on melanocytes or indirect effects via keratinocytes and on the transfer of melanosomes. They also help to sustain hyperpigmentation by increasing the number of blood vessels and, in turn, the level of endothelin‐1.

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“…Ultraviolet‐induced skin pigmentation is regulated by interactions between melanocytes and neighboring cells, such as keratinocytes or fibroblasts . Specifically, an important role of photoaged fibroblasts in the development of UV‐associated hyperpigmentary disorders, solar lentigo or melasma has been suggested . In addition to fibroblasts, growing evidence also implicates blood vessels in pigmentation .…”

Section: Introductionmentioning

confidence: 99%

Increased blood flow and vasculature in solar lentigo

Hasegawa

Fujiwara

Satô

et al. 2016

The Journal of Dermatology

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Solar lentigo (SL) is a hallmark of ultraviolet (UV)-induced photoaged skin and growing evidence implicates blood vessels in UV-associated pigmentation. In this study, we investigated whether the vasculatures are modified in SL. Twenty-five women with facial SL were enrolled and colorimetric and blood flow studies were performed. There was a significant increase in erythema which was associated with increased blood flow in the lesional skin compared with perilesional normal skin. Immunohistochemical studies with 24 facial SL biopsies consistently revealed a significant increase in vessel density accompanied by increased levels of vascular endothelial growth factor expression. CD68 immunoreactivity was significantly higher in lesional skin suggesting increased macrophage infiltration in SL. In conclusion, SL is characterized by increased blood flow and vasculature. These findings suggest the possible influence of the characteristics of vasculature on development of SL.

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Factors secreted by irradiated aged fibroblasts induce solar lentigo in pigmented reconstructed epidermis

Cited by 42 publications

References 10 publications

Clonogenic Cell Subpopulations Maintain Congenital Melanocytic Nevi

Clonogenic Cell Subpopulations Maintain Congenital Melanocytic Nevi

How hormones may modulate human skin pigmentation in melasma: An in vitro perspective

Increased blood flow and vasculature in solar lentigo

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