期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 118, 期 4, 页码 718-725出版社
WILEY
DOI: 10.1002/jcb.25676
关键词
CORTISOL; NON-GENOMIC; STRESS; TELEOST; SKELETAL MUSCLE; MYOTUBE
资金
- Fondo Nacional de Desarrollo Cientifico y Tecnologico [1130545]
- CONICYT/FONDAP [15110027]
- UNAB [DI-1277-16/R]
Cortisol is an essential regulator of neuroendocrine stress responses in teleosts. Cortisol predominantly affects target tissues through the genomic pathway, which involves interacting with cytoplasmic glucocorticoid receptors, and thereby, modulating stress-response gene expressions. Cortisol also produces rapid effects via non-genomic pathways, which do not involve gene transcription. Although cortisolmediated genomic pathways are well documented in teleosts, non-genomic pathways are not fully understood. Moreover, no studies have focused on the contribution of non-genomic cortisol pathways in compensatory stress responses in fish. In this study, rainbow trout (Oncorhynchus mykiss) skeletal myotubes were stimulated with physiological concentrations of cortisol and cortisol-BSA, a membrane impermeable agent, resulting in an early induction of reactive oxygen species (ROS). This production was not suppressed by transcription or translation inhibitors, suggesting non-genomic pathway involvement. Moreover, myotube preincubation with RU486 and NAC completely suppressed cortisol- and cortisol-BSA induced ROS production. Subcellular fractionation analysis revealed the presence of cell membrane glucocorticoid receptors. Finally, cortisol-BSA induced a significant increase in ERK1/2 and CREB phosphorylation, as well as in CREB dependent transcriptional activation of the pgc1a gene expression. The obtained results strongly suggest that cortisol acts through a nongenomic glucocorticoid receptor-mediated pathway to induce ROS production and contribute to ERK/CREB/PGC1-alpha signaling pathway activation as stress compensation mechanisms. (C) 2016 Wiley Periodicals, Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据