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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 >Effect of Abeta exposure on the mRNA expression patterns of voltage-sensitive calcium channel alpha1 subunits (alpha1A-alpha1D) in human SK-N-SH neuroblastoma.
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Effect of Abeta exposure on the mRNA expression patterns of voltage-sensitive calcium channel alpha1 subunits (alpha1A-alpha1D) in human SK-N-SH neuroblastoma.

机译：Abeta暴露对人SK-N-SH神经母细胞瘤中电压敏感钙通道alpha1亚基（alpha1A-alpha1D）mRNA表达模式的影响。

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摘要

Evidence for loss of Ca(2+) homeostasis through voltage-sensitive Ca(2+) channels (VSCCs) contribution to neuronal degeneration induced by beta-amyloid protein (Abeta) is considerable and rapidly increasing. Thus, the expression patterns of four alpha(1) subunits for P/Q (alpha(1A))-, N (alpha(1B))-, and L (alpha(1C) and alpha(1D))-type VSCCs before and after Abeta exposure were investigated in human SK-N-SH neuroblastoma. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed a constitutive and abundant co-expression of mRNA for alpha(1A) and alpha(1D) subunit in control cells. The mRNA expression of another L-type subunit alpha(1C) was undetectable in control cells while N-type subunit alpha(1B) was relative lower when compared to alpha(1A) and alpha(1D) subunits. Interestingly, mRNA levels of alpha(1A), alpha(1B), and alpha(1C) were remarkably and time-dependently increased in response to Abeta (20 microM) for 72 h culture period. In contrast, the constitutively expressed alpha(1D)mRNA was not further modified during Abeta exposure. Western blot analysis of four alpha(1) subunits expression was consistent with the findings obtained by RT-PCR. In conclusion, our results suggested that P/Q-, N-, as well as L-type Ca(2+) channel genes might be existed in SK-N-SH cells. Among them, mRNA for alpha(1A), alpha(1B), and alpha(1D) were expressed constitutively while alpha(1C) were inducible. Furthermore, Abeta exposure selectively modulates the transcription of alpha(1A), alpha(1B), and alpha(1C) subunits. These suggested that except activating of existed VSCCs, up-regulation of alpha(1) subunits expression might also contribute to Abeta-induced neuronal toxicity and the complex of these VSCCs expression may participate in Ca(2+) current disturbance in Alzheimer's disease.
机译：通过电压敏感的Ca（2+）通道（VSCCs）对由β-淀粉样蛋白（Abeta）诱导的神经元变性的作用引起的Ca（2+）稳态丧失的证据是相当可观的，并且迅速增加。因此，之前的P / Q（alpha（1A））-，N（alpha（1B））-和L（alpha（1C）和alpha（1D））型VSCC的四个alpha（1）亚基的表达模式并且在人SK-N-SH神经母细胞瘤中研究了Abeta暴露后的情况。逆转录聚合酶链反应（RT-PCR）分析表明，在控制细胞中，alpha（1A）和alpha（1D）亚基的mRNA组成性丰富。当与alpha（1A）和alpha（1D）亚基相比时，在对照细胞中无法检测到另一个L型亚基alpha（1C）的mRNA表达，而N型亚基alpha（1B）相对较低。有趣的是，响应Abeta（20 microM）72小时的培养时间，α（1A），α（1B）和α（1C）的mRNA水平显着且随时间增加。相反，在Abeta暴露过程中，组成型表达的alpha（1D）mRNA未被进一步修饰。四个alpha（1）亚基表达的蛋白质印迹分析与通过RT-PCR获得的发现一致。总之，我们的结果表明，SK-N-SH细胞中可能存在P / Q-，N-以及L型Ca（2+）通道基因。其中，alpha（1A），alpha（1B）和alpha（1D）的mRNA组成性表达，而alpha（1C）则可诱导。此外，Abeta暴露选择性地调节alpha（1A），alpha（1B）和alpha（1C）亚基的转录。这些表明，除了激活现有的VSCC，α（1）亚基表达的上调也可能导致Abeta诱导的神经元毒性，并且这些VSCC表达的复合物可能参与了Alzheimer病的Ca（2+）当前紊乱。

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