Chemotherapy-induced alopecia is a major problem in clinical oncology. Doxorubicin, a widely used cancer chemotherapy drug, induces disruption of the hair cycle and subsequent alopecia. We show in this report that doxorubicin causes disruption of the hair-follicle-associated blood vessel network resulting in a greatly reduced density of these blood vessels. Dystrophic hair follicles were also observed with abnormal melanogenesis in the mice treated with doxorubicin. Visualization of the effect of doxorubicin on hair-follicle angiogenesis was made possible by the use of transgenic mice in which green fluorescent protein was driven by regulatory elements of the nestin gene (ND-GFP). In these transgenic mice, the hair-follicle stem cells and the follicle structure as well as the blood vessels associated with the hair follicles express ND-GFP. The hair-follicle stem cells did not appear to be affected by doxorubicin, which may explain why hair regrows after chemotherapy. These results suggest that inhibition of hair-follicle-associated angiogenesis by doxorubicin may be an important factor in hair-follicle dystrophy associated with chemotherapy-induced alopecia. The ND-GFP mouse model is thus useful for the study of the role of angiogenesis in the hair-follicle cycle and the effect of drugs on processes associated with chemotherapy-induced alopecia.

译文

化学疗法引起的脱发是临床肿瘤学中的主要问题。阿霉素是一种广泛使用的癌症化学治疗药物,可引起毛发周期破坏和随后的脱发。我们在这份报告中表明,阿霉素会导致毛囊相关血管网络的破坏,从而导致这些血管的密度大大降低。在用阿霉素治疗的小鼠中还观察到营养不良的毛囊黑色素生成异常。通过使用其中巢蛋白基因(ND-GFP)调控元件驱动绿色荧光蛋白的转基因小鼠,可以看到阿霉素对毛囊血管生成的作用。在这些转基因小鼠中,毛囊干细胞,毛囊结构以及与毛囊相关的血管均表达ND-GFP。毛囊干细胞似乎没有受到阿霉素的影响,这可以解释为什么化疗后头发会长大。这些结果表明,阿霉素抑制与毛囊相关的血管生成可能是与化学疗法引起的脱发有关的毛囊营养不良的重要因素。因此,ND-GFP小鼠模型可用于研究血管生成在毛囊周期中的作用以及药物对与化学疗法引起的脱发相关的过程的作用。

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