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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The p38(MAPK) signaling pathway regulates neuronal apoptosis through the phosphorylation of the retinoblastoma protein.
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The p38(MAPK) signaling pathway regulates neuronal apoptosis through the phosphorylation of the retinoblastoma protein.

机译：p38（MAPK）信号通路通过视网膜母细胞瘤蛋白的磷酸化调节神经元凋亡。

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摘要

We investigated the role of SB202190, a selective p38 mitogen-activated protein kinase (MAPK) inhibitor in cerebellar granule neurons (CGC) in response to serum potassium deprivation (S/K deprivation), an apoptotic stimulus. CGC apoptosis after S/K deprivation was shown to be mediated through cell cycle re-entry and the induction of transcription factor E2F-1. We found that SB 202190 (10muM) inhibits retinoblastoma protein (pRb) phosphorylation, in response to S/K deprivation. Moreover, the expression of cyclin E and E2F-1 were also significantly decreased. Interestingly, SB202190 did not affect or modulate the increase in the protein expression levels of cyclin D1. Similarly, p-Akt and p-GSK3 protein levels, measured after 12h S/K deprivation, did not appear to be regulated by SB 202190 (10muM). These data indicate that the neuroprotective effects of the p38 inhibitor were not mediated via Akt activation. In conclusion, these results suggest that p38MAPK converged with the cell cycle in S/K deprivation-induced apoptosis through pRb phosphorylation.
机译：我们调查了SB202190，选择性p38丝裂原激活的蛋白激酶（MAPK）抑制剂在小脑颗粒神经元（CGC）中对血清钾缺乏（S / K缺乏）（一种细胞凋亡刺激）的反应中的作用。 S / K剥夺后的CGC细胞凋亡被证明是通过细胞周期再进入和转录因子E2F-1的诱导介导的。我们发现SB 202190（10μM）抑制视网膜母细胞瘤蛋白（pRb）磷酸化，以响应S / K剥夺。此外，细胞周期蛋白E和E2F-1的表达也显着降低。有趣的是，SB202190不会影响或调节细胞周期蛋白D1蛋白表达水平的增加。同样，S / K剥夺12h后测得的p-Akt和p-GSK3蛋白水平似乎不受SB 202190（10μM）的调节。这些数据表明，p38抑制剂的神经保护作用不是通过Akt激活介导的。总之，这些结果表明，p38MAPK通过pRb磷酸化与S / K剥夺诱导的细胞凋亡收敛于细胞周期。

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