Expression analysis of actin-related genes as an underlying mechanism for mood disorders
Expression analysis of actin-related genes as an underlying mechanism for mood disorders
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DOI：
10.1016/j.bbrc.2006.11.101
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发表时间：
2007-01-19
影响因子：
3.1
通讯作者：
Yoshikawa, Takeo
中科院分区：
文献类型：
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作者：
Nakatani, Noriaki;Ohnishi, Tetsuo;Yoshikawa, Takeo
在这项研究中，我们探索了新提出的情绪障碍“细胞骨架紊乱”理论。首先，通过结合我们之前的遗传和当前全基因组表达分析的结果，我们将肌动蛋白周转的重要调节因子基因Cap1确定为小鼠抑郁性状的有效数量性状基因。然后，我们严格检查了 C5713L/6 (136)（易患抑郁症）和 C3H/He (C3)（抗抑郁症）小鼠额叶皮质中“核心”肌动蛋白相关基因的表达。我们证实 Cap1 在 B6 中的转录物和蛋白质水平上均下调。其他差异调节的基因包括 cofilin I 和 profilin I（在 136 中上调）和 Rho 家族 GTPase 成员 (Pak1)（在 136 中下调）。第三，我们研究了人类死后前额皮质中的“核心”肌动蛋白通路成分，并观察了双极大脑中 CAP1 减少的趋势。这些数据表明，在情绪障碍中，肌动蛋白动力学的平衡可能会朝着肌动蛋白解聚的方向改变。 (c) 2006 Elsevier Inc. 保留所有权利。
In this study, we explored the newly postulated 'disturbed cytoskeletal' theory of mood disorders. Firstly, we identified Cap1, a gene for important mediator of actin turnover, as a cogent quantitative trait gene for depressive trait of mice by combining the results of our prior genetic and current genome-wide expression analyses. Then we rigorously examined 'core' actin-related gene expression in the frontal cortex of C5713L/6 (136) (prone to depression) and C3H/He (C3) (resistant to depression) mice. We confirmed that Cap1 was down-regulated at both transcript and protein levels in B6. Other differentially regulated genes included cofilin I and profilin I (up-regulated in 136), and a Rho-family GTPase member (Pak1) (down-regulated in 136). Thirdly, we investigated the 'core' actin-pathway components in human postmortem prefrontal cortices, and observed trend for CAP1 reduction in the bipolar brains. These data suggest that the balance of actin dynamics might be altered towards actin depolymerization in mood disorders. (c) 2006 Elsevier Inc. All rights reserved.