Embryo exposure to elevated cortisol level leads to cardiac performance dysfunction in zebrafish
Embryo exposure to elevated cortisol level leads to cardiac performance dysfunction in zebrafish
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DOI：
10.1016/j.mce.2012.07.010
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发表时间：
2012-11-05
影响因子：
4.1
通讯作者：
Vijayan, Mathilakath M.
中科院分区：
文献类型：
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作者：
Nesan, Dinushan;Vijayan, Mathilakath M.
在斑马鱼(Danio Rerio)中，新星皮质醇的合成只有在孵化后才开始，这为研究母体应激和皮质醇异常沉积对胚胎发育和性能的影响提供了一个有趣的模型。我们假设，在孵化前胚胎发生期间，皮质醇水平升高会损害斑马鱼发育过程中的心脏功能。将皮质醇显微注射到单细胞胚胎中，以提高胚胎发生期间的基础皮质醇水平。胚胎皮质醇含量升高会增加心脏畸形，包括心包水肿和心腔畸形，并在孵化后降低静息心跳。这种表型与心脏关键基因的抑制相吻合，包括NKX2.5、心肌肌球蛋白轻链1、心肌肌钙蛋白T2A型和钙转运ATPase，这支持了心脏畸形的机制联系。孵化后对次级应激源的心跳反应的减弱也证实了心脏功能的下降。总而言之，胚胎发育过程中皮质醇含量过高，类似于母体应激导致的沉积增加，会降低心脏功能，并可能降低斑马鱼后代的存活率。(C)2012爱思唯尔爱尔兰有限公司。保留所有权利。
In zebrafish (Danio rerio), de nova cortisol synthesis commences only after hatching, providing an interesting model to study the effects of maternal stress and abnormal cortisol deposition on embryo development and performance. We hypothesized that elevated cortisol levels during pre-hatch embryogenesis compromise cardiac performance in developing zebrafish. Cortisol was microinjected into one-cell embryos to elevate basal cortisol levels during embryogenesis. Elevated embryo cortisol content increased heart deformities, including pericardial edema and malformed chambers, and lowered resting heartbeat post-hatch. This phenotype coincided with suppression of key cardiac genes, including nkx2.5, cardiac myosin light chain 1, cardiac troponin type T2A, and calcium transporting ATPase, underpinning a mechanistic link to heart malformation. The attenuation of the heartbeat response to a secondary stressor post-hatch also confirms a functional reduction in cardiac performance. Altogether, high cortisol content during embryogenesis, mimicking increased deposition due to maternal stress, decreases cardiac performance and may reduce zebrafish offspring survival. (C) 2012 Elsevier Ireland Ltd. All rights reserved.