Modulation of endothelin‐1 in normal human keratinocytes by UVA1/B radiations, prostaglandin E2 and peptidase inhibitors

Pernet, Ingrid; Mayoux, C.; Trompezinski, S.; Schmitt, D; Viac, J.

doi:10.1034/j.1600-0625.2000.009006401.x

Cited by 13 publications

(16 citation statements)

References 17 publications

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“…In contrast, UVB led to an increase of bFGF and ET‐1, but did not alter the production of the other growth factors. The reduction of ET‐1 protein by UVA in contrast to the upregulation of ET‐1 protein by UVB is in accordance with previous reports 23,26 , 27 . However, Pernet et al 26 .…”

Section: Discussionsupporting

confidence: 92%

“…The reduction of ET-1 protein by UVA in contrast to the upregulation of ET-1 protein by UVB is in accordance with previous reports. 23,26,27 However, Pernet et al 26 while we observed a marked increase in ET-1 mRNA expression by UVB and a slight increase by UVA 12 h after irradiation. This discrepancy between the UVA-induced increase in ET-1 mRNA, but decrease in ET-1 protein, suggests that UVA may have inhibited ET-1 at the post-transcriptional level, for example by suppressing the secretion of protein.…”

Section: Discussioncontrasting

confidence: 52%

“…The reduction of ET‐1 protein by UVA in contrast to the upregulation of ET‐1 protein by UVB is in accordance with previous reports 23,26 , 27 . However, Pernet et al 26 . could not find a quantitative change in ET‐1 mRNA expression 4 and 6 h after irradiation with UVA and UVB, while we observed a marked increase in ET‐1 mRNA expression by UVB and a slight increase by UVA 12 h after irradiation.…”

Section: Discussionmentioning

confidence: 99%

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Differential expression of melanoma-associated growth factors in keratinocytes and fibroblasts by ultraviolet A and ultraviolet B radiation

et al. 2005

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UVA and UVB can stimulate and inhibit the production of growth factors for melanocytes in keratinocytes and fibroblasts dependent on the cell type and wavelength. We show for the first time that UVA and UVB can activate bFGF, HGF and TGF-beta1 in fibroblasts, while bFGF was the most inducible factor both in fibroblasts and in keratinocytes. The induction of bFGF and HGF in fibroblasts by UVA suggests that stroma cells in the dermis may be involved in the UV activation of melanocytes via paracrine ways and thus promote melanoma development.

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Section: Discussionsupporting

confidence: 92%

Section: Discussioncontrasting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

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Differential expression of melanoma-associated growth factors in keratinocytes and fibroblasts by ultraviolet A and ultraviolet B radiation

et al. 2005

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“…Confirming recent in vitro data and findings in the skin of human and mouse skin that expression and release of ET-1 is markedly enhanced in response to UVB, 9,16,25,29 we show that ET-1 concentrations in UVB-irradiated skin increase more than 13-fold above baseline levels. This UV-mediated increase in ET-1 levels is associated with augmented skin inflammation resulting, in part, from MCs activated by 4 These differences reflect the ability of MCs to either promote homeostasis and, thus, to diminish pathology (eg, by degrading endogenous or exogenous toxins through the release of proteases) 4 or to induce pathology (eg, by releasing potent proinflammatory mediators such as tumor necrosis factor-␣, histamine, leukotrienes, and many more).…”

Section: Discussionsupporting

confidence: 74%

Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

Metz¹,

Lammel²,

Gibbs

et al. 2006

The American Journal of Pathology

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Endothelin (ET-1) has been shown to crucially contribute to UV-induced skin responses such as tanning.To test whether ET-1 is also involved in early cutaneous reactions to UV, we assessed ET-1 skin levels in UV-irradiated mice. In correlation with the levels of UV-induced skin inflammation, ET-1 concentrations increased substantially and continually. Moreover, blocking of ET-1 receptors (ET A ) resulted in significantly decreased cutaneous inflammation following UV irradiation. When we assessed skin responses to ET-1 injections, we observed prominent mast cell degranulation and mast cell-dependent inflammation. Since mast cells also critically contributed to UV-induced inflammation, we determined the ET-1-dependent inflammatory response to UV in the absence and presence of these cells. Interestingly, ET A blockade did not decrease UV-induced inflammation in mast cell-deficient mice, unless these mice had been adoptively transferred with mast cells before irradiation. This indicates that skin inflammation due to UV irradiation is caused in part by ET-1 acting on skin mast cells. Immediate skin responses following exposure to sunlight are largely mediated by UV-B light (UVB): low to moderate doses of UVB result in tanning, whereas intense UVB irradiation also gives rise to considerable inflammation, ie, solar dermatitis. UVB-induced tanning is widely regarded to result from the up-regulation of pigment production in epidermal melanocytes, which is induced by melanogens released from activated keratinocytes. In contrast, the cellular and molecular mechanisms involved in the induction of inflammatory skin responses to UVB are largely unknown.Recently, the vasoconstrictor peptide endothelin-1 (ET-1), one of the melanogens that contributes to UVBinduced tanning, 1,2 was found to promote inflammation in various pathological processes. For example, we and others have recently shown that ET-1 levels are up-regulated in murine septic peritonitis and that elevated ET-1 levels contribute to morbidity and mortality in this setting.3,4 Increased ET-1 production and mRNA expression have been demonstrated in lung tissue and bronchoalveolar lavage fluid in different models of airway inflammation. [5][6][7] In addition, elevated ET-1 concentrations are also present in patients with systemic lupus erythematosus, Takayasu arteritis, or Raynaud's phenomenon, where, in the latter case, the increase was shown clearly to contribute to disease severity. 8 These observations indicate that ET-1, in addition to having stimulatory effects on melanocytes, may orchestrate the induction of inflammatory responses after UVB irradiation. Two recent reports support this notion. First, the expression of ET-1 and its receptors ET A and ET B in murine skin was found to be markedly and rapidly upregulated after UVB irradiation, both in the dermis and epidermis.9 Second, intracutaneous injections of ET-1 reportedly trigger inflammatory reactions, including a pronounced flare response associated with sensations of a burning itch, a classic symptom of a ...

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“…10 Other compounds may be also utilized to affect the ET-1 autocrine loop by reducing ET-1 synthesis, such as inhibitors of ET-1 converting enzyme. 11 In conclusion, we have shown some indications for the development of new therapeutic strategies in psoriatic patients by altering the biological response of keratinocytes to the ET-1 proliferative stimuli. These new therapies would not affect the pathological causes of this skin disorder but could reduce and stabilize the symptoms that are the major problem of patients with this disease.…”

mentioning

confidence: 84%

Endothelin-1 could be one of the targets of psoriasis therapy

et al. 2004

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Modulation of endothelin‐1 in normal human keratinocytes by UVA1/B radiations, prostaglandin E2 and peptidase inhibitors

Cited by 13 publications

References 17 publications

Differential expression of melanoma-associated growth factors in keratinocytes and fibroblasts by ultraviolet A and ultraviolet B radiation

Differential expression of melanoma-associated growth factors in keratinocytes and fibroblasts by ultraviolet A and ultraviolet B radiation

Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

Endothelin-1 could be one of the targets of psoriasis therapy

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