毛囊外根鞘中E6和E7乳头瘤病毒癌基因的表达延长了生长期,绕过了休止期。

D Escalante-Alcalde, F Recillas-Targa, C Valencia, J Santa-Olalla, P Chávez, A Marroquín, Gutiérrez-X, P Gariglio, L Covarrubias
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引用次数: 0

摘要

毛囊生长周期经历了一系列严格控制细胞增殖、分化和细胞死亡的阶段。在外根鞘(ORS)中表达人乳头瘤病毒16型E6/E7乳头瘤病毒致癌基因的转基因小鼠表现出毛发密度较低、再生毛发能力比野生型小鼠快的毛发表型。转基因小鼠再生毛囊的生长期(生长期)较长,虽然毛囊退化(毛囊退化)发生,但未观察到休止期休息。在毛囊生长的第一个周期中没有发现异常,但在第二个周期中,毛囊生长的开始延迟,休止期休息也没有达到,即使有雌二醇(休止期休息信号)存在。综上所述,在转基因小鼠中,表达E6/E7延缓了ORS进入休止期,使ORS细胞对持续毛囊循环的休止期休息信号不敏感。
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Expression of E6 and E7 papillomavirus oncogenes in the outer root sheath of hair follicles extends the growth phase and bypasses resting at telogen.

Hair follicle growth cycle proceeds through a series of stages in which strict control of cell proliferation, differentiation, and cell death occurs. Transgenic mice expressing human papillomavirus type 16 E6/E7 papillomavirus oncogenes in the outer root sheath (ORS) display a fur phenotype characterized by lower hair density and the ability to regenerate hair much faster than wild-type mice. Regenerating hair follicles of transgenic mice show a longer growth phase (anagen), and although bulb regression (catagen) occurs, rest at telogen was not observed. No abnormalities were detected during the first cycle of hair follicle growth, but by the second cycle, initiation of catagen was delayed, and rest at telogen was again not attained, even in the presence of estradiol, a telogen resting signal. In conclusion, expression of E6/E7 in the ORS delays entrance to catagen and makes cells of the ORS insensitive to telogen resting signals bearing to a continuous hair follicle cycling in transgenic mice.

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