Do hair bulb melanocytes undergo apoptosis during hair follicle regression (catagen)?
Do hair bulb melanocytes undergo apoptosis during hair follicle regression (catagen)?
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DOI：
10.1046/j.1523-1747.1998.00417.x
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发表时间：
1998-12
期刊：
影响因子：
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通讯作者：
D. Tobin;Evelin Hagen;V. Botchkarev;Ralf Paus
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文献类型：
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作者：
D. Tobin;Evelin Hagen;V. Botchkarev;Ralf Paus
生长期毛囊周期性退化过程中毛囊色素单位的命运尚不清楚。利用C57BL/6小鼠毛发研究模型，观察毛囊黑素细胞在生发-退变过程中的变化，比较自发和药物诱导的退变过程中黑素细胞的发育。这项研究表明，自发性和地塞米松诱导的增生剂在色素单位中显示出类似的变化。退化性毛囊在毛乳头和选定的外根鞘角质形成细胞中表现出色素失禁。在自发性增生体和地塞米松诱导的增生性增生体中检测到因凋亡而被删除的黑素细胞，并在透射电子显微镜下通过缺乏上皮特化的受影响细胞中存在游离的前黑素小体以及TUNEL阳性和酪氨酸酶相关蛋白-1免疫反应的共同定位来鉴定。相比之下，环磷酰胺诱导的退行性变的特征是在广泛的角质形成细胞凋亡存在的情况下，黑素细胞和树突状黑素细胞最初保留。黑素细胞大小便失禁和黑色素的异位分布比其他类型的退行性变更严重。虽然这些黑色素大部分是通过毛管挤出到皮肤表面的，但在表皮中也检测到了毛囊衍生的色素，可能来自近端毛囊中携带色素的外根鞘角质形成细胞。因此，细胞凋亡可能至少在一定程度上是自发性衰老过程中黑素细胞丧失的原因。虽然地塞米松诱导的退行性变可能为一般毛发色素沉着的研究提供了有用的模型，但环磷酰胺诱导的退行性变为研究黑素细胞对化学损伤的反应和相对抵抗力提供了一个有趣的模型。
The fate of the hair follicle pigmentary unit during the cyclical involution of anagen hair follicles is unknown. Using the C57BL/6 mouse model for hair research, hair follicle melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and pharmacologically induced catagen development. This study shows that both spontaneous catagen and dexamethasone-induced catagen display similar changes in the pigmentary unit. Catagen hair follicles exhibited pigment incontinence in the dermal papilla and in selected outer root sheath keratinocytes. Melanocytes deleted by apoptosis were detected in spontaneous catagen and, more commonly, in dexamethasone-induced catagen, and were identified using transmission electron microscopy by the presence of free premelanosomes in affected cells lacking epithelial specializations, and by the colocalization of TUNEL positivity and tyrosinase-related protein-1 immunoreactivity. By contrast, cyclophosphamide-induced catagen was characterized by the initial retention of melanogenic and dendritic melanocytes in the presence of widespread keratinocyte apoptosis. Melanocyte incontinence and the ectopic distribution of melanin were more severe than in the other forms of catagen. Whereas much of this melanin was extruded, via the hair canal, to the skin surface, hair follicle-derived pigment was also detected within the epidermis, probably derived from pigment-carrying migrating outer root sheath keratinocytes from the proximal hair follicle. Thus, apoptosis may account, at least in part, for the loss of melanogenic melanocytes during spontaneous catagen. Although dexamethasone-induced catagen may provide a useful model for general hair pigmentation research, catagen induced by cyclophosphamide offers an interesting model for studying the response, and relative resistance, of melanocytes to chemical injury.