各位战友好，有不当之处，敬请批评指出，谢谢！ / ]2 Q' M% ^" _% ` / y' K7 S; `* t5 _* W成人牙髓干细胞的电离辐射可引起P53的激活、细胞周期的停止和细胞衰老，但不引起细胞凋亡! c) O, W/ ~6 {3 t: \$ v1 Z
7 g6 [, T& ~3 e; m' O0 v! K M( b0 O8 `2 i来源出版物: STEM CELLS AND DEVELOPMENT 卷: 19 期: 12 页: 1855-1862 出版年: DEC 2010 - y r( c) \$ r& b! Y, J
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摘要：成人牙髓干细胞（DPSCs）可以分化成成骨细胞、成牙本质细胞、成脂肪细胞和神经元样细胞。因为这些细胞在组织再生中有很大的潜力，所以我们描述DPSCs在电离辐射（IR）下的反应。实验中所用的DPSCs是从健康成人的磨牙中得到的。DPSCs在一个含有表皮生长因子（EGF）和血小板源性生长因子（PDGF）的培养基中进行培养。由于组织生长的动态平衡是依赖于细胞增殖、衰老及死亡间的精细平衡，我们探索研究IR剂量2-20Gy对DPSCs的增殖效率以及增殖过程所涉及的分子通路的影响。尽管IR剂量达到最大（20Gy），仍然没有引起DPSCs凋亡。IR（6和20Gy）后，于细胞周期G2收集DPSCs。在IR20Gy的第三天，DPSCs检测到sa -β-半乳糖苷酶阳性，提示其发生衰老。照射后24小时，能检测到P53及其15和392磷酸化形式。在这个时候，P21（WAF1）被诱导。蛋白P16从照射第三天开始产生，并持续到照射结束（第十三天）。我们得出结论：在IR破坏下，DPSCs的细胞周期永久性停止于G2期，并由于压力产生过早的衰老。5 b1 u9 i- u+ i
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附上摘要原文： ! M5 y- H$ \! B; \6 ?0 t: ~Irradiation of Adult Human Dental Pulp Stem Cells Provokes Activation of p53, Cell Cycle Arrest, and Senescence but Not Apoptosis $ i k3 Y; Y5 z1 \, |8 v" z
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摘要: Adult human dental pulp contains stem cells (DPSCs) that are capable of differentiation into osteoblasts, odon-toblasts, adipocytes, and neuronal-like cells. Because these cells have potential use in tissue regeneration, herein we characterized the response of DPSC lines to ionizing radiation (IR). These DPSC lines have been developed from the extracted molars of healthy donors. DPSCs were cultivated in a unique media supplemented with epidermal growth factor (EGF) and platelet-derived growth factor (PDGF). Since tissue homeostasis depends on a precise balance among cell proliferation, senescence, and cell death, we explored the effects of IR (2-20 Gy) on the proliferative activity of DPSCs and the molecular pathways involved. Even the highest dose used (20 Gy) did not induce DPSC apoptosis. After irradiation with doses of 6 and 20 Gy, DPSCs accumulated in the G2 phase of the cell cycle. DPSCs responded to IR (20 Gy) with senescence detected as SA-beta-galactosidase positivity, beginning on the third day after irradiation. Twenty-four hours after irradiation, p53 and its serine 15 and 392 phosphorylated forms were detected. At this time, p21 (WAF1) was induced. Increases in protein p16 were observed from the third day following irradiation and continued till the end of the examination (Day 13). We conclude that DPSCs respond to IR-induced damage by permanent cell cycle arrest in the G2 phase and by stress-induced premature senescence.$ K* d1 ]# ]5 m+ a