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首页> 外文期刊>Journal of Cellular Physiology >Mitotic cycle reactivation in terminally differentiated cells by adenovirus infection.
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Mitotic cycle reactivation in terminally differentiated cells by adenovirus infection.

机译：细胞周期激活在晚期分化细胞腺病毒感染。

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摘要

Different cell types (e.g., neurons, skeletal and heart myocytes, adipocytes, keratinocytes) undergo terminal differentiation, in which acquisition of specialized functions entails definitive withdrawal from the cell cycle. Such cells are distinct from quiescent (reversibly growth-arrested) cells, such as contact-inhibited fibroblasts. Terminally differentiated cells can not be induced to proliferate by means of growth factor stimulation or transduction of cellular oncogenes. An important first step toward defining the molecular basis for such unresponsiveness is to find a practical means to overcome the proliferative block. Furthermore, determining whether terminally differentiated, postmitotic cells still retain a potential competence for proliferation that can be reactivated would have important theoretical and practical implications. To address these questions, we exploited the properties of adenoviruses. These viruses can infect postmitotic cells and express E1A, a powerful activator of proliferation in reversibly growth-arrested cells. We infected terminally differentiated skeletal muscle cells and adipocytes with human adenovirus type 5 or 12, obtaining full reentry into the cell cycle, including DNA synthesis, mitosis, cytokinesis, and extended proliferation. Similar results were obtained with established cell lines and primary cells belonging to several species, from quail to humans. Genetic analysis indicated that the smaller splice product of E1A, E1A 12S, is sufficient to induce cell cycle reactivation in otherwise permanently nonmitotic cells. These results demonstrate that terminally differentiated cells retain proliferative potential and establish adenovirus as a convenient and powerful means to force such cells to reenter the cell cycle.
机译：不同的细胞类型(如神经、骨骼和心脏细胞,脂肪细胞,角质细胞)进行终端分化,收购需要专门的功能明确的退出细胞周期。细胞不同于静(可逆growth-arrested)细胞,如contact-inhibited成纤维细胞。不诱导增殖的增长因素刺激或转导的细胞致癌基因。定义的分子基础反应迟钝是找到一种实用的手段克服增生性的块。决定终末分化,postmitotic细胞仍保留潜力的增殖能力将有着重要的理论和复发实际意义。问题,我们利用的特性腺病毒。postmitotic细胞和表达E1A,强大在可逆催化剂的扩散growth-arrested细胞。分化和骨骼肌细胞脂肪细胞与人类腺病毒类型5到12日获得完整的再入进入细胞周期,包括DNA合成、有丝分裂、胞质分裂,和扩展扩散。获得建立细胞系和主属于几个物种的细胞,从鹌鹑人类。较小的拼接E1A的产物,E1A 12年代,足以诱导细胞周期激活否则永久nonmitotic细胞。结果表明,晚期分化细胞具有增殖潜力,建立腺病毒作为一个方便和强大的手段迫使这些细胞重新进入细胞周期。

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