Caldesmon, an actin-linked regulatory protein, comes across glucocorticoids
Caldesmon, an actin-linked regulatory protein, comes across glucocorticoids
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Caldesmon 是一种肌动蛋白连接的调节蛋白，与糖皮质激素相结合
DOI：
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发表时间：
2010
影响因子：
3.2
通讯作者：
Kentaro Fukumoto
中科院分区：
文献类型：
--
作者：
K. Sobue;Kentaro Fukumoto
糖皮质激素(GCs)是下丘脑-垂体-肾上腺(HPA)轴最下游的效应物质，是应激反应的主要介质。应激触发的GC以及急慢性GC治疗会损害大脑的结构可塑性和功能。围产期动物和人类暴露在过度应激或GC下会影响大脑发育，导致动物成年后代的行为改变，并增加人类精神疾病的风险。尽管有大量研究记录了这些影响，但其潜在机制仍不清楚。在这篇评论中，我们将重点关注过多的GC对皮质发育的影响。我们最近发现，过度依赖GC的神经前体细胞径向迁移的延迟是由于肌动蛋白-肌球蛋白相互作用的失调，通过上调肌动蛋白连接的调节蛋白钙调蛋白(CAD)。阐明糖皮质激素对大脑皮层发育不利作用的分子机制将有助于我们理解应激/糖皮质激素如何改变神经网络的形成并影响生命后期的行为。
The glucocorticoids (GCs), the most downstream effectors of the hypothalamus-pituitary-adrenal (HPA) axis, are the main mediators of stress response. Stress-triggered GCs as well as acute and chronic GC treatment can impair the structural plasticity and function of the brain. The exposure of perinatal animals and humans to excess stress or GCs can affect the brain development, resulting in altered behaviors in the adult offspring of animals and an increased risk of psychiatric disorders in humans. Despite the numerous studies documenting these effects, the underlying mechanism remains unclear. In this commentary we will focus on the effect of excess GCs on cortical development. We have recently showed that excess-GC-dependent retardation of the radial migration of neural progenitor cells (NPCs) is caused by the dysregulation of actin-myosin interaction via upregulation of caldesmon (CaD), an actin-linked regulatory protein. The elucidation of the molecular mechanisms that underlie the detrimental action of GCs on cortical development will expand our understanding of how stress/GCs alter the formation of neural networks and affect behaviors later in life.
DOI：
10.1152/ajpregu.2002.282.1.r55
发表时间：
2002-01-01
影响因子：
2.8
作者：
Flagel, SB;V치zquez, DM;Neal, CR
通讯作者：
Neal, CR
影响因子：
3.3
作者：
Lo, CM;Buxton, DB;Wang, YL
通讯作者：
Wang, YL
影响因子：
9.8
作者：
McEwen, BS
通讯作者：
McEwen, BS