Non-segmental vitiligo (NSV) is an acquired chronic pigmentation disorder characterized by depigmented macules of various sizes with tendency toward symmetrical distribution [1] and [2]. Despite many studies performed on vitiligo skin, the exact pathogenesis of this dermatosis is still to be clarified. Recently, it has been suggested that the major and possible primary predisposing factor in vitiligo development could be a defective adhesion of melanocytes and that mechanical trauma and various chemical stressors could represent the main precipitating events [3] and [4]. Interactions between melanocytes and the basement membrane are mediated by different molecules [5] and particularly by integrin alpha5beta1 (a5b1int) [6]. The lack of a5b1int's adhesive role caused by trauma or chemical stressors could be the first pathological step that leads to vitiligo. This first step, anyway, is never observed in normal skin, even if trauma or chemical stressor could be present. So, a sort of priming factor could be operative in order to develop the vitiliginous patches. “Melanoma inhibitory activity” (MIA) is a small protein secreted from malignant melanoma cells [7]. It has been demonstrated that MIA interacts with a5b1int [8] by binding to this protein at cell surface and modulating integrin activity and thereby causing the detachment of melanoma cells from extracellular matrix proteins. We investigated the expression of MIA in vitiliginous skin and its relationship with a5b1int in order to further clarify the pathogenesis of this dermatosis.

Role of alpha5beta1 integrin and MIA (melanoma inhibitory activity) in the pathogenesis of vitiligo.

BORDIGNON, MATTEO;CASTELLANI, CHIARA;FEDRIGO, MARNY;THIENE, GAETANO;PESERICO STECCHINI NEGRI DE SALVI, ANDREA;ALAIBAC, MAURO SALVATORE ALESSANDRO;ANGELINI, ANNALISA
2013

Abstract

Non-segmental vitiligo (NSV) is an acquired chronic pigmentation disorder characterized by depigmented macules of various sizes with tendency toward symmetrical distribution [1] and [2]. Despite many studies performed on vitiligo skin, the exact pathogenesis of this dermatosis is still to be clarified. Recently, it has been suggested that the major and possible primary predisposing factor in vitiligo development could be a defective adhesion of melanocytes and that mechanical trauma and various chemical stressors could represent the main precipitating events [3] and [4]. Interactions between melanocytes and the basement membrane are mediated by different molecules [5] and particularly by integrin alpha5beta1 (a5b1int) [6]. The lack of a5b1int's adhesive role caused by trauma or chemical stressors could be the first pathological step that leads to vitiligo. This first step, anyway, is never observed in normal skin, even if trauma or chemical stressor could be present. So, a sort of priming factor could be operative in order to develop the vitiliginous patches. “Melanoma inhibitory activity” (MIA) is a small protein secreted from malignant melanoma cells [7]. It has been demonstrated that MIA interacts with a5b1int [8] by binding to this protein at cell surface and modulating integrin activity and thereby causing the detachment of melanoma cells from extracellular matrix proteins. We investigated the expression of MIA in vitiliginous skin and its relationship with a5b1int in order to further clarify the pathogenesis of this dermatosis.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2577966
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