期刊
AGING CLINICAL AND EXPERIMENTAL RESEARCH
卷 25, 期 3, 页码 231-238出版社
SPRINGER
DOI: 10.1007/s40520-013-0045-6
关键词
Heat stress; Vascular endothelial cell; Telomere; Subtelomere; DNA methylation
资金
- Ministry of Education, Science, and Culture of Japan [23590885]
- National Natural Science Fund (NSFC) [81170329/H2501]
- Health and Labour Sciences Research Grants Comprehensive Research on LifeStyle Related Diseases including Cardiovascular Diseases and Diabetes Mellitus
- Grants-in-Aid for Scientific Research [23591083, 23590885] Funding Source: KAKEN
Temperature-associated alteration in the telomere lengths of vascular endothelial cells has not been well investigated. Telomere length of human umbilical vein endothelial cells (HUVECs) cultured at a high temperature (42 degrees C) was analyzed. Here described are heat-associated phenotypical alterations of human vascular endothelial cell under prolonged heat stress in terms of telomere length, telomerase activity, and the expression of telomere associated proteins and heat shock proteins. The genomic DNA extracted from HUVECs cultured for 3 days under 42 degrees C was digested with methylation-sensitive and-insensitive isoschizomers and was subjected to genomic Southern blot probed with a telomere DNA fragment. Their telomere lengths and telomere length distributions were analyzed. Telomerase activity and the expressions of telomere-associated RNA, telomere-associated proteins (TERC, TERT, TRF1, and TRF2), and heat shock proteins (Hsp60, Hsp70, and Hsp90) were also analyzed. At 42 degrees C, cell growth was suppressed and the cell senescence rate was transiently elevated. A proportional decrease in the number of long telomeres was observed transiently at 42 degrees C. A trend of subtelomeric hypomethylation and lowered telomerase activity were observed at 42 degrees C after 3-day culture. The altered phenotypes on day 1 seemed reactive responses for cell protection to heat, and those on day 3 seemed exhausted reactions after 3-day culture. Maintained expression was observed in Hsps, TRF2, and TERC. These altered phenotypes might contribute to cell-survival under prolonged heat stress.
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