The impact of acute temperature stress on hemocytes of invasive and native mussels (Mytilus galloprovincialis and Mytilus californianus): DNA damage, membrane integrity, apoptosis and signaling pathways
The impact of acute temperature stress on hemocytes of invasive and native mussels (Mytilus galloprovincialis and Mytilus californianus): DNA damage, membrane integrity, apoptosis and signaling pathways
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DOI：
10.1242/jeb.073577
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发表时间：
2012-12-01
影响因子：
2.8
通讯作者：
Somero, George N.
中科院分区：
文献类型：
--
作者：
Yao, Cui-Luan;Somero, George N.
我们分别研究了急性热应激和冷应激对本地贻贝和入侵贻贝（Mytilus californianus和Mytilus galloprovincialis）血细胞活力、溶酶体膜稳定性、双链和单链DNA断裂以及细胞稳态和凋亡的信号机制的影响。热应激（28,32摄氏度）和冷应激（2,6摄氏度）都会导致DNA的双链和单链断裂。DNA损伤的类型和程度取决于温度和时间，caspase-3激活是细胞凋亡的一个指标，可能发生在DNA损伤的反应中。热应激显著降低血细胞活力和溶酶体膜稳定性。细胞信号和应激反应相关蛋白（包括磷酸化特异性丝裂原活化蛋白激酶（MAPK）家族成员c-JUN nh2末端激酶（JNK）和p38-MAPK，以及凋亡执行子caspase-3）的抗体的白细胞提取物的Western blot分析显示，冷热应激诱导JNK、p38-MAPK和caspase-3的时间依赖性激活，并且这些信号和应激反应在物种之间存在差异。与应力诱导损伤修复相关的细胞信号过程激活的热极限可能有助于确定细胞的热耐受极限。我们的研究结果显示了对冷应激和热应激的相似反应，并表明在极端温度下DNA损伤水平与下游调节反应（包括诱导凋亡）之间存在因果关系。与加利福尼亚栗鼠相比，加galloprovincialis可能由于单双链DNA损伤量更少、信号激活和转导更快、对温度胁迫的修复能力更强而具有更广泛的耐温性。
We investigated the effects of acute heat stress and cold stress on cell viability, lysosome membrane stability, double- and single-stranded DNA breakage, and signaling mechanisms involved in cellular homeostasis and apoptosis in hemocytes of native and invasive mussels, Mytilus californianus and Mytilus galloprovincialis, respectively. Both heat stress (28, 32 degrees C) and cold stress (2, 6 degrees C) led to significant double- and single-stranded breaks in DNA. The type and extent of DNA damage were temperature and time dependent, as was caspase-3 activation, an indicator of apoptosis, which may occur in response to DNA damage. Hemocyte viability and lysosomal membrane stability decreased significantly under heat stress. Western blot analyses of hemocyte extracts with antibodies for proteins associated with cell signaling and stress responses [including members of the phospho-specific mitogen-activated protein kinase (MAPK) family c-JUN NH2-terminal kinase (JNK) and p38-MAPK, and apoptosis executor caspase-3] revealed that heat and cold stress induced a time-dependent activation of JNK, p38-MAPK and caspase-3 and that these signaling and stress responses differed between species. The thermal limits for activation of cell signaling processes linked to the repair of stress-induced damage may help determine cellular thermal tolerance limits. Our results show similarities in responses to cold and heat stress and suggest causal linkages between levels of DNA damage at both extremes of temperature and downstream regulatory responses, including induction of apoptosis. Compared with M. californianus, M. galloprovincialis might have a wider temperature tolerance due to a lower amount of single-and double-stranded DNA damage, faster signaling activation and transduction, and stronger repair ability against temperature stress.