Juvenile Xanthogranuloma and Neurofibromatosis 1

Tan, Hiok‐Hee; Tay, Yong Kwang

doi:10.1159/000017974

Cited by 22 publications

(15 citation statements)

References 6 publications

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“…PPARγ was not detectable by this method. In both freshly dispersed (relatively mature) and cultured (relatively immature) adult rat epidermal cells, PPARδ mRNA was more highly expressed than PPARα mRNA (Deplewski, unpublished data), and PPARγ mRNA was not detected by RNase protection assay [17, 18]. Parallel results have been been obtained in cultured human keratinocytes [32].…”

Section: Ppar Gene Expression In Normal Skinmentioning

confidence: 76%

“…PPARα and PPARγ activators were found to stimulate lipid droplet accumulation in cultured immature sebocytes, but not in keratinocytes, as assessed histochemically using Oil Red O staining in cells cultured under high calcium conditions [17, 18]. PPARγ activation induced a greater degree of sebocyte colony differentiation than PPARα activation and significantly enhanced the differentiative response of sebocytes to androgen.…”

Section: Effects Of Ppar Activators On Cultured Epidermal and Sebaceomentioning

confidence: 99%

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Peroxisome Proliferator-Activated Receptors and Skin Development

2000

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PPARs are nuclear hormone receptors. PPAR subtypes (α, γ, δ, the latter a xPPARβ homologue) were initially investigated in skin because of their known role in regulating lipid metabolism. Studies adding specific PPAR ligand activators to cultured skin or skin cells are compatible with the concepts that PPARα activation mediates early lipogenic steps common to the function of both skin epidermal cells (keratinocytes) and sebaceous cells (sebocytes), PPARγ activation plays a unique role in stimulating sebocyte lipogenesis, and PPARδ activation may contribute to lipid biosynthesis in both sebocytes and keratinocytes under certain circumstances. Epidermal keratinocytes appear to express small amounts of PPARα and PPARδ mRNA and a trace of PPARγ mRNA which is up-regulated with differentiation. Sebocytes express all subtypes; PPARγ gene expression excedes that in epidermis. The emerging data on PPAR protein expression suggests that epidermis normally expresses predominantly PPARα, while sebocytes express more PPARγ than PPARα. These expression patterns may change during hyperplasia, differentiation and inflammation. Gene disruption studies in mice are compatible with a contribution of PPARα to skin barrier function, suggest that PPARγ is necessary for sebocyte differentiation, and indicate that PPARδ can ameliorate inflammatory responses in skin. PPARs appear to play a role in keratinocyte synthesis of the lipids that they export to the intercellular space to form the skin permeability barrier. They also appear to be important for sebocyte formation of the intracellular fused lipid droplets that constitute the holocrine secretion of the sebaceous gland. In addition, they may play roles in keratinocyte growth and differentiation and the inhibition of skin inflammation by diverse mechanisms not necessarily related to fat metabolism.

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Section: Ppar Gene Expression In Normal Skinmentioning

confidence: 76%

Section: Effects Of Ppar Activators On Cultured Epidermal and Sebaceomentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptors and Skin Development

2000

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“…In addition, there is evidence that the effect of androgens on human sebocyte proliferation depends on the area of skin from which the sebaceous glands are obtained; facial sebocytes are mostly affected [84, 88]. Androgens have also been shown to stimulate sebocyte differentiation [89]which is augmented by co-incubation with PPARγ ligands [90]. Dermal papilla cells mediate the growth-stimulating signals of androgens by releasing growth factors that act in a paracrine fashion on the other cells of the follicle [6, 87].…”

Section: Biological Activity Of Hormones In Human Skinmentioning

confidence: 99%

“…IL1α expression has been detected in follicular keratinocytes and sebocytes in vivo and in vitro [73, 110, 111, 112]. Interestingly, LTB 4 is a natural ligand for PPARα [113, 114], soluble 15-HETE, which is a natural ligand for PPAR-γ [115], is synthesized in human sebaceous glands [116], and PPARs can regulate lipid and lipoprotein metabolism, cell proliferation, differentiation and apoptosis of various cell types including sebocytes [90]. The axis IL-1/LTB 4 /PPARα/lipid synthesis and inflammation was confirmed by a current clinical study; treatment of acne patients with a specific 5-lipoxygenase inhibitor administered systemically led to a 70% reduction in inflammatory acne lesions at 3 months, an approximately 65% reduction in total sebum lipids as well as a substantial decrease in proinflammatory lipids [117].…”

Section: Biological Activity Of Hormones In Human Skinmentioning

confidence: 99%

Human Skin: An Independent Peripheral Endocrine Organ

2000

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The historical picture of the endocrine system as a set of discrete hormone-producing organs has been substituted by organs regarded as organized communities in which the cells emit, receive and coordinate molecular signals from established endocrine organs, other distant sources, their neighbors, and themselves. In this wide sense, the human skin and its tissues are targets as well as producers of hormones. Although the role of hormones in the development of human skin and its capacity to produce and release hormones are well established, little attention has been drawn to the ability of human skin to fulfil the requirements of a classic endocrine organ. Indeed, human skin cells produce insulin-like growth factors and -binding proteins, propiomelanocortin derivatives, catecholamines, steroid hormones and vitamin D from cholesterol, retinoids from diet carotenoids, and eicosanoids from fatty acids. Hormones exert their biological effects on the skin through interaction with high-affinity receptors, such as receptors for peptide hormones, neurotransmitters, steroid hormones and thyroid hormones. In addition, the human skin is able to metabolize hormones and to activate and inactivate them. These steps are overtaken in most cases by different skin cell populations in a coordinated way indicating the endocrine autonomy of the skin. Characteristic examples are the metabolic pathways of the corticotropin-releasing hormone/propiomelanocortin axis, steroidogenesis, vitamin D, and retinoids. Hormones exhibit a wide range of biological activities on the skin, with major effects caused by growth hormone/insulin-like growth factor-1, neuropeptides, sex steroids, glucocorticoids, retinoids, vitamin D, peroxisome proliferator-activated receptor ligands, and eicosanoids. At last, human skin produces hormones which are released in the circulation and are important for functions of the entire organism, such as sex hormones, especially in aged individuals, and insulin-like growth factor-binding proteins. Therefore, the human skin fulfils all requirements for being the largest, independent peripheral endocrine organ.

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“…35,36 Several studies have performed direct sequencing for BRAF-V600E, and most failed to identify any cases of JXG with the mutation. In our institutional series, we did identify 2 patients with disseminated histiocytic disease with some lesions with characteristics of LCH, as well as JXG with the BRAF-V600E mutation.…”

Section: Molecular Landscape Of Jxgmentioning

confidence: 99%