Plasma corticosterone activates SGK1 and induces morphological changes in oligodendrocytes in corpus callosum.
Plasma corticosterone activates SGK1 and induces morphological changes in oligodendrocytes in corpus callosum.
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DOI：
10.1371/journal.pone.0019859
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Tohyama M
中科院分区：
文献类型：
--
作者：
Miyata S;Koyama Y;Takemoto K;Yoshikawa K;Ishikawa T;Taniguchi M;Inoue K;Aoki M;Hori O;Katayama T;Tohyama M
已知反复的压力事件与抑郁症的发作有关。此外，应激通过升高血浆皮质醇水平激活下丘脑-垂体-肾上腺皮质（HPA）系统。然而，对相关的下游分子途径知之甚少。在本研究中，通过使用重复水浸和束缚应激（WIRS）作为应激源的小鼠，我们试图阐明血浆皮质酮水平升高诱导的分子途径。我们在体内和体外观察到以下效应：（1）重复暴露于WIRS激活3-磷酸肌醇依赖性蛋白激酶（PDK 1）-血清糖皮质激素调节激酶（SGK 1）-N-myc下游调节基因1（NDRG 1）-粘附分子（即，N-钙粘蛋白、α-连环蛋白和β-连环蛋白）稳定通路;（2）该信号通路的激活诱导少突胶质细胞的形态学变化;（3）从慢性应激中恢复后，少突胶质细胞的异常树枝化和抑郁样症状恢复到对照水平。我们的数据有力地表明，这些异常的少突胶质细胞可能与抑郁样症状。
Repeated stressful events are known to be associated with onset of depression. Further, stress activates the hypothalamic–pituitary–adrenocortical (HPA) system by elevating plasma cortisol levels. However, little is known about the related downstream molecular pathway. In this study, by using repeated water-immersion and restraint stress (WIRS) as a stressor for mice, we attempted to elucidate the molecular pathway induced by elevated plasma corticosterone levels. We observed the following effects both, in vivo and in vitro: (1) repeated exposure to WIRS activates the 3-phosphoinositide-dependent protein kinase (PDK1)–serum glucocorticoid regulated kinase (SGK1)–N-myc downstream-regulated gene 1 (NDRG1)–adhesion molecule (i.e., N-cadherin, α-catenin, and β-catenin) stabilization pathway via an increase in plasma corticosterone levels; (2) the activation of this signaling pathway induces morphological changes in oligodendrocytes; and (3) after recovery from chronic stress, the abnormal arborization of oligodendrocytes and depression-like symptoms return to the control levels. Our data strongly suggest that these abnornalities of oligodendrocytes are possibly related to depression-like symptoms.
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影响因子：
3.7
作者：
Kachhap SK;Faith D;Qian DZ;Shabbeer S;Galloway NL;Pili R;Denmeade SR;DeMarzo AM;Carducci MA
通讯作者：
Carducci MA
影响因子：
3.3
作者：
Fraser, M. M.;Bayazitov, I. T.;Baker, S. J.
通讯作者：
Baker, S. J.
影响因子：
2.8
作者：
Koyama, Yoshihisa;Fujiwara, Toshihiro;Tohyama, Masaya
通讯作者：
Tohyama, Masaya
影响因子：
17.7
作者：
Kendler, KS;Karkowski, LM;Prescott, CA
通讯作者：
Prescott, CA
影响因子：
2.3
作者：
Leussis, Melanie P.;Andersen, Susan L.
通讯作者：
Andersen, Susan L.