TERT enhances the survival rate of human fibroblasts under endoplasmic reticulum, Golgi apparatus, and lysosomal stresses.

TERT enhances the survival rate of human fibroblasts under endoplasmic reticulum, Golgi apparatus, and lysosomal stresses.
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TERT 提高人成纤维细胞在内质网、高尔基体和溶酶体应激下的存活率。

DOI:
10.1007/s10529-018-2544-1
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发表时间:
2018
影响因子:
2.7
通讯作者:
Ozawa K
Ozawa K
中科院分区:
工程技术4区
文献类型:
--
作者:
Abd El-Hafeez AA;Hosoi T;Nakatsu K;Thon M;Shimamoto A;Tahara H;Ozawa K

文献摘要

相似文献

细胞器,如内质网(ER),高尔基体(GA)和溶酶体暴露于应激激活死亡机制。最近,端粒酶逆转录酶(TERT)已被证明参与细胞存活。然而,端粒酶逆转录酶与应激反应的关系仍不清楚。在这里,我们的目的是阐明可能的作用机制,通过研究其对人类成纤维细胞中多个细胞器所面临的压力的影响,通过TERT促进细胞存活。结果我们发现,无论ER应激诱导剂如衣霉素,TERT都能提高ER应激下细胞的存活率(蛋白糖基化抑制剂)、毒胡萝卜素(Ca 2 +-ATP酶抑制剂)、布雷菲德菌素A(蛋白转运抑制剂)或二硫苏糖醇(二硫键形成抑制剂)。我们还发现,TERT增强GA和溶酶体stress. Collectively下的细胞存活率,这些结果表明,TERT抑制细胞应激,促进细胞存活通过不同的机制。这些发现可能为TERT在治疗应激诱导的疾病(如衰老、肥胖和神经退行性疾病)方面的意义提供新的见解。
ObjectiveThe exposure of organelles, such as the endoplasmic reticulum (ER), Golgi apparatus (GA), and lysosomes, to stress activates death mechanisms. Recently, telomerase reverse transcriptase (TERT) has been shown to be involved in cell survival. However, the relationship between TERT and the stress responses is still unclear. Here, we aimed to clarify the possible mechanisms of action through which TERT promotes cell survival by studying its effect on the stresses faced by multiple organelles in human fibroblasts.ResultsWe found that TERT enhanced the survival rate of cells under ER stress, regardless of ER stress inducers such as tunicamycin (protein glycosylation inhibitor), thapsigargin (Ca2+-ATPase inhibitor), brefeldin A (protein transport inhibitor), or dithiothreitol (disulfide bond formation inhibitor). We also found that TERT enhanced the survival rate of cells under GA and lysosomal stresses.ConclusionCollectively, these results suggest that TERT suppresses cell stress and promotes cell survival via different mechanisms. These findings may offer new insights into the implications of TERT in the treatment of stress-induced conditions such as aging, obesity, and neurodegenerative diseases.