Activation of Akt is induced by heat shock and involved in suppression of heat-shock-induced apoptosis of NIH3T3 cells
Activation of Akt is induced by heat shock and involved in suppression of heat-shock-induced apoptosis of NIH3T3 cells
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DOI：
10.1006/bbrc.2000.3805
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发表时间：
2000-11-19
影响因子：
3.1
通讯作者：
Kang, SS
中科院分区：
文献类型：
--
作者：
Bang, OS;Ha, BG;Kang, SS
NIH3T3细胞在45度高温下暴露15分钟，可激活由pi3激酶介导的Akt， pi3激酶特异性抑制剂可显著抑制热休克诱导的磷酸化。磷酸化的Akt在热休克后9 h内逐渐降低至基础水平。这导致生长停滞，但在24 h内细胞可以恢复生长并具有较高的增殖率。而热休克60 min后，Akt未被激活，导致细胞凋亡。热休克诱导激活Akt后细胞生长的恢复被wortmannin完全阻断。此外，Akt显性阴性突变体的过表达显著抑制热休克对细胞凋亡的抑制作用，表明热休克诱导的Akt激活直接参与细胞凋亡抑制。提示NIH3T3细胞热休克后，pi3激酶/Akt信号转导通路可能具有抑制细胞凋亡的功能。(C) 2000年学术出版社。
Heat shock exposure to NIH3T3 cells for 15 min at 45 degreesC activated Akt, which is mediated by PI3-kinase, as evidenced by the significant inhibition of heat-shock-induced phosphorylation by specific inhibitors of PI3-kinase. The phosphorylated Akt was gradually decreased to the basal level within 9 h after heat shock. This resulted in growth arrest, but cell growth could be recovered within 24 h accompanied with a high rate of proliferation. However, heat shock for 60 min failed to activate Akt, resulting in apoptosis. The recovery of cell growth after heat-shock-inducing activation of Akt was completely blocked by wortmannin. Moreover, overexpression of a dominant-negative Akt mutant significantly inhibited the apoptosis-suppressive effect of heat shock, indicating the direct involvement of heat-shock-induced Akt activation in the apoptosis suppression. The results indicate that a signal transduction pathway, namely, PI3-kinase/Akt, may contribute to an apoptosis-suppressive function after heat shock in NIH3T3 cells. (C) 2000 Academic Press.