Altered pattern of growth and differentiation in human keratinocytes infected by simian virus 40.
Altered pattern of growth and differentiation in human keratinocytes infected by simian virus 40.
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被猿猴病毒 40 感染的人角质形成细胞的生长和分化模式发生改变。
DOI：
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发表时间：
1979
影响因子：
11.1
通讯作者：
V. Defendi
中科院分区：
文献类型：
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作者：
M. Steinberg;V. Defendi
用猴病毒40体外感染人表皮角质形成细胞。发育中的角质形成细胞集落的结构反映了完整皮肤中细胞分裂和角质化的空间分离;胸腺嘧啶掺入细胞主要位于集落殖民地外围，而非分裂的组织学分化细胞聚集在内部。病毒感染导致增殖群体的规模急剧增加，同时，殖民地内部的分化减少。当猴病毒40 T抗原合成仅在一小部分细胞中检测到时，这些变化是明显的;随着T抗原阳性细胞的百分比在连续传代中上升，分化变得越来越依赖于密度。生长/分化定位的正常模式的破坏与生长对血清的依赖性的丧失相一致，但在与转化相关的其他病毒诱导性质的出现之前;即，在软琼脂中形成集落的能力和不依赖于成纤维细胞的生长。
Human epidermal keratinocytes were infected by simian virus 40 in vitro. The structure of the developing keratinocyte colony reflects the spatial separation of cell division and keratinization in intact skin; thymidine-incorporating cells were primarily localized at the colony periphery whereas nondividing, histologically differentiated cells accumulated in the interior. Viral infection produced a dramatic increase in the size of the proliferative population as, simultaneously, differentiation was reduced in the colony interior. These changes were manifest when simian virus 40 T-antigen synthesis was detectable in only a small percentage of the cells; differentiation became increasingly density dependent as the percentage of T-antigen-positive cells rose over serial passage. The disruption of the normal pattern of growth/differentiation localization coincided with a loss of dependence on serum for growth, but preceded the appearance of other virus-induced properties associated with transformation; i.e., the ability to form colonies in soft agar and independence of growth from fibroblasts.