Keratinocyte cultures from involved skin in vitiligo patients show an impaired in vitro behaviour
Keratinocyte cultures from involved skin in vitiligo patients show an impaired in vitro behaviour
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DOI：
10.1111/j.1600-0749.2007.00385.x
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发表时间：
2007-08-01
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影响因子：
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通讯作者：
Guerra, Liliana
中科院分区：
文献类型：
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作者：
Bondanza, Sergio;Maurelli, Riccardo;Guerra, Liliana
白癜风色素脱失被认为是受累区域黑素细胞消失或功能丧失的结果。然而，有报道称，白癜风患者皮肤中的角质形成细胞也受到了损害。基于这一证据，我们在生命周期培养中评估了受累和非受累白斑角质形成细胞的体外行为及其增殖、分化和衰老标记物的表达。另一个目的是研究来自脱色皮肤的白癜风角质形成细胞是否能够维持正常黑素细胞的存活和生长(在共培养实验中加入时)，就像正常人角质形成细胞所做的那样。我们的结果表明，几乎所有受累的白斑角质形成细胞在体外的寿命都比未受累的细胞短，而且它们在培养中都不能维持黑素细胞的生理比例。增殖和衰老标记物的表达也会发生改变。事实上，我们检测到白癜风角质形成细胞中衰老标记物p16的初始表达水平较低，尽管它们的体外寿命较短，而增殖细胞核抗原和p53的表达增加。这项对少量体外培养的白癜风角质形成细胞的初步分析表明，白癜风角质形成细胞的衰老过程受损，并试图对其进行调节。
Vitiligo depigmentation is considered a consequence of either melanocyte disappearance or loss of functioning melanocytes in the involved areas. However, it has been reported that keratinocytes in involved vitiligo skin are damaged too. Based on this evidence, we evaluated the in vitro behaviour, in life span cultures, of involved and uninvolved vitiligo keratinocytes and their expression of proliferation, differentiation and senescence markers. An additional purpose was to investigate whether vitiligo keratinocytes from depigmented skin are able to sustain survival and growth of normal melanocytes (when added in co-culture experiments), as normal human keratinocytes manage to do. Our results demonstrate that almost all involved vitiligo keratinocytes have a shorter life span in vitro than the uninvolved cells and all of them do not maintain melanocytes in culture in a physiological ratio. Modification of proliferation and senescence marker expression also occurs. Indeed, we detected low initial expression levels of the senescence marker p16 in involved vitiligo keratinocytes, despite their shorter in vitro life span, and increased expression of proliferating cell nuclear antigen and p53. This preliminary analysis of a small number of in vitro cultured vitiligo keratinocytes suggests an impaired senescence process in lesional vitiligo keratinocytes and attempts to regulate it.