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Dehydration stress alters the mitogen-activated-protein kinase signaling and chaperone stress response in Xenopus laevis.
Comparative Biochemistry and Physiology B: Biochemistry & Molecular Biology ( IF 2.2 ) Pub Date : 2020-06-01 , DOI: 10.1016/j.cbpb.2020.110461
Cheng-Wei Wu 1 , Shannon N Tessier 2 , Kenneth B Storey 3
Affiliation  

In arid conditions, the African Clawed frog Xenopus laevis enters a state of estivation dormancy as an adaptive survival strategy. Under estivation, X. laevis experience severe dehydration stress as 25–35% of total body water is lost. Dehydration in X. laevis can lead to periods of hypoxia due to elevated blood viscosity that impedes tissue perfusion. To understand how X. laevis survives under such stress, we studied the regulation pattern of key mitogen-activated protein kinases (MAPK) and their downstream transcription factors, along with several heat shock proteins in the oxygen sensitive brain and heart tissue of X. laevis under dehydration stress. Our study revealed that the activation phosphorylation residues of MAPK including JNK and MSK and their downstream transcription factors c-Jun and ATF2 are significantly decreased in the heart under dehydration. Given that JNK, c-Jun, and ATF2 are known positive regulators of apoptosis, this regulatory pattern suggest that a state of pro-survival signals may be established in the dehydrated heart. In support of this, protein levels of HSP60, a pro-apoptotic mitochondrial chaperone, was also downregulated in the heart in response to dehydration stress. In the brain tissue, most proteins remain unchanged with the exception of the apoptosis regulating p53 transcription factor, which showed a significant decrease in its activating phosphorylation residue under dehydration. Overall, our study revealed that in the Xenopus brain and heart, a specific suppression pattern of MAPK, transcription factors, and HSP takes place to potentially establish a state of pro-survival under dehydration stress.



中文翻译:

脱水应激会改变非洲爪蟾的促分裂原活化蛋白激酶信号传导和伴侣应激反应。

在干旱条件下,非洲爪蛙Xenopus laevis进入了休眠休眠状态,作为一种适应性生存策略。在耕作下,X。laevis遭受了严重的脱水压力,因为损失了25%至35%的体内总水分。X. laevis中的脱水可能会导致缺氧期,这是由于血液粘度升高阻止了组织灌注。为了了解X. laevis如何在这种压力下生存,我们研究了关键丝裂原激活蛋白激酶(MAPK)及其下游转录因子的调控模式,以及X. laevis对氧敏感的大脑和心脏组织中的几种热激蛋白在脱水压力下。我们的研究表明,脱水后心脏中的MAPK的激活磷酸化残基(包括JNK和MSK及其下游转录因子c-Jun和ATF2)显着降低。鉴于JNK,c-Jun和ATF2是已知的凋亡正调节剂,这种调节模式表明在脱水的心脏中可能建立了生存信号的状态。支持这一点的是,心脏中的HSP60(一种促凋亡的线粒体伴侣)的蛋白质水平也因脱水应激而在心脏中下调。在脑组织中,除凋亡调节p53转录因子外,大多数蛋白质保持不变,后者在脱水状态下其活化磷酸化残基显着减少。总体而言,我们的研究表明,非洲爪蟾的大脑和心脏,MAPK,转录因子和HSP的特定抑制模式发生,以潜在地建立脱水压力下的生存前状态。

更新日期:2020-06-01
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