Dynamin and myosin regulate differential exocytosis from mouse adrenal chromaffin cells.
Dynamin and myosin regulate differential exocytosis from mouse adrenal chromaffin cells.
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DOI：
10.1007/s10571-010-9591-z
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发表时间：
2010-11
影响因子：
4
通讯作者：
Smith, Corey
中科院分区：
文献类型：
--
作者：
Chan, Shyue-An;Doreian, Bryan;Smith, Corey
肾上腺髓质的神经内分泌嗜铬细胞代表交感神经系统的主要输出。嗜铬细胞通过大的致密核心分泌颗粒的胞吐融合将儿茶酚胺以及血管和神经活性肽递质释放到循环中。在基础交感神经活动下，嗜铬细胞选择性地释放适度水平的儿茶酚胺，帮助设置能量储存的“休息和消化”状态。在应激激活下，升高的交感神经放电导致增加的儿茶酚胺以及肽递质释放，以设置能量消耗的“战斗或逃跑”状态。虽然儿茶酚胺释放的机制已被广泛研究，但对肽递质释放如何在升高的刺激下被调节以选择性地发生知之甚少。最近的研究表明，在基础刺激下选择性释放儿茶酚胺是通过颗粒和质膜之间的短暂的、受限的胞吐融合孔来实现的，释放小的、可扩散的分子的可溶性部分。升高的细胞放电导致融合孔的主动扩张，导致释放儿茶酚胺和扩散性较低的肽递质。在这里，我们提出了一个分子机制，调节活性依赖性扩张的融合孔。我们回顾了直接的文献，并提供了新的数据，制定一个工作机制的假设，即钙介导的去磷酸化的发动蛋白I在Ser-774导致招聘的分子运动肌球蛋白II积极扩张的融合孔，以促进肽递质的释放。因此，动力蛋白的活性依赖性去磷酸化被假设为交感-肾上腺应激反应中的关键分子步骤。
Neuroendocrine chromaffin cells of the adrenal medulla represent a primary output for the sympathetic nervous system. Chromaffin cells release catecholamine as well as vaso- and neuro-active peptide transmitters into the circulation through exocytic fusion of large dense-core secretory granules. Under basal sympathetic activity, chromaffin cells selectively release modest levels of catecholamines, helping to set the “rest and digest” status of energy storage. Under stress activation, elevated sympathetic firing leads to increased catecholamine as well as peptide transmitter release to set the “fight or flight” status of energy expenditure. While the mechanism for catecholamine release has been widely investigated, relatively little is known of how peptide transmitter release is regulated to occur selectively under elevated stimulation. Recent studies have shown selective catecholamine release under basal stimulation is accomplished through a transient, restricted exocytic fusion pore between granule and plasma membrane, releasing a soluble fraction of the small, diffusible molecules. Elevated cell firing leads to the active dilation of the fusion pore, leading to the release of both catecholamine and the less diffusible peptide transmitters. Here we propose a molecular mechanism regulating the activity-dependent dilation of the fusion pore. We review the immediate literature and provide new data to formulate a working mechanistic hypothesis whereby calcium-mediated dephosphorylation of dynamin I at Ser-774 leads to the recruitment of the molecular motor myosin II to actively dilate the fusion pore to facilitate release of peptide transmitters. Thus, activity-dependent dephosphorylation of dynamin is hypothesized to represent a key molecular step in the sympatho-adrenal stress response.
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DOI：
10.1111/j.1749-6632.2002.tb04489.x
发表时间：
2002-01-01
期刊：
CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND INFORMATICS
影响因子：
--
作者：
Cavadas, C;Silva, AP;Grouzmann, E
通讯作者：
Grouzmann, E
影响因子：
3
作者：
Fulop, Tiberiu;Smith, Corey
通讯作者：
Smith, Corey
影响因子：
25
作者：
Anggono, Victor;Smillie, Karen J;Graham, Mark E;Valova, Valentina A;Cousin, Michael A;Robinson, Phillip J
通讯作者：
Robinson, Phillip J
影响因子：
3.4
作者：
Chen, P;Gillis, KD
通讯作者：
Gillis, KD
DOI：
10.1523/jneurosci.1976-09.2009
发表时间：
2009-06-17
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Clayton EL;Anggono V;Smillie KJ;Chau N;Robinson PJ;Cousin MA
通讯作者：
Cousin MA