Reversible changes in the nuclear lamina induced by hyperthermia.

Reversible changes in the nuclear lamina induced by hyperthermia.
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高温引起核层的可逆变化。

DOI:
10.1002/jcb.10241
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发表时间:
2002
期刊:
Journal of cellular biochemistry.
影响因子:
--
通讯作者:
Dynlacht,JosephR
Dynlacht,JosephR
中科院分区:
--
文献类型:
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作者:
Falloon,ElizabethA;Dynlacht,JosephR

文献摘要

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核基质(NM)已被确定为热诱导细胞杀伤的潜在靶标。先前的研究表明,热休克可能显著调节层粘胶蛋白B的含量。由于纳米结构的变化通常伴随着蛋白质组成的变化,我们研究了高温是否会诱导非耐高温和耐高温细胞的核层(NL)结构的变化,以及这些变化对细胞存活的影响。使用间接免疫荧光技术和共聚焦显微镜,我们发现在42或45.5°C下加热细胞会导致外周NL内陷和其他畸变。虽然热疗不会改变内部层粘连蛋白B灶的数量或结构,但热诱导的外周NL的改变是剂量依赖性的。有趣的是,在注定存活或死亡的细胞中,NL结构在加热后随着时间的推移而恢复。与非耐高温细胞相比,在45.5℃下加热的耐高温细胞NL的初始变化相似,但恢复速度要快得多。综上所述,这些结果表明外周NL的初始损伤量与热诱导的细胞杀伤无关。然而,提高康复率可能带来生存优势的可能性不容忽视。j .细胞。生物化学学报,26(6):451 - 456,2002。©2002 Wiley‐Liss, Inc。
The nuclear matrix (NM) has been identified as a potential target for heat‐induced cell killing. Previous studies have shown that heat‐shock may significantly modulate lamin B content. Since changes in NM structure have often been accompanied by changes in protein composition, we investigated whether hyperthermia induced changes in nuclear lamina (NL) structure in non‐tolerant and thermotolerant cells, and the implications of these changes on cell survival. Using indirect immunofluorescence techniques and confocal microscopy, we found that heating cells at 42 or 45.5°C caused invaginations and other distortions of the peripheral NL. While hyperthermia did not alter the number or structure of internal lamin B foci, heat‐induced alterations to the peripheral NL were dose‐dependent. Interestingly, NL structure recovered with time after heating in cells that were destined to live or die. Thermotolerant cells heated at 45.5°C showed similar initial changes in the NL compared to non‐tolerant cells, but recovery occurred much faster. Taken together, these results suggest that the amount of initial damage to the peripheral NL is not correlated with heat‐induced cell killing. However, the possibility that an increased rate of recovery might confer a survival advantage cannot be discounted. J. Cell. Biochem. 86: 451–460, 2002. © 2002 Wiley‐Liss, Inc.