Avoidance of apoptosis in embryonic cells of the annual killifish Austrofundulus limnaeus exposed to anoxia.
Avoidance of apoptosis in embryonic cells of the annual killifish Austrofundulus limnaeus exposed to anoxia.
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DOI：
10.1371/journal.pone.0075837
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Podrabsky JE
中科院分区：
文献类型：
--
作者：
Meller CL;Podrabsky JE
一年生鳉鱼的胚胎 在脊椎动物中，澳底鱼具有无与伦比的长期缺氧生存能力。令人惊讶的是，这些胚胎可以在缺氧中存活数月，尽管在缺氧暴露的最初几个小时内ATP水平大规模下降。已知这些病症由于缺血或缺氧而触发哺乳动物细胞中的凋亡性细胞死亡。缺氧诱导的凋亡诱导在四个发育阶段进行了研究， A . limnaeus的缺氧耐受性不同，因此可能对缺氧有独特的反应。暴露于星形孢菌素用于确定是否 A . Limnaeus细胞有能力通过除缺氧以外的线索进入凋亡。凋亡细胞通过TUNEL分析和通过测量半胱天冬酶3/7活性来鉴定。暴露于48小时的缺氧没有诱导TUNEL阳性细胞的增加，一般不会导致caspase 3/7活性的增加。然而，用10 μM星形孢菌素处理缺氧胚胎导致常氧和缺氧胚胎中caspase 3/7活性显著增加。这些结果表明，细胞凋亡是避免在胚胎 A . limnaeus暴露于缺氧后的细胞凋亡至少部分是通过阻止caspase 3/7活性活化的机制实现的。虽然这种机制仍然未知，但它可能是由一种蛋白激酶触发的，这种蛋白激酶可以通过实验被星形孢菌素抑制。
Embryos of the annual killifish Austrofundulus limnaeus have unequalled ability among vertebrates to survive long-term anoxia. Surprisingly, these embryos can survive for months in anoxia despite a large-scale decrease in ATP levels during the initial hours of anoxic exposure. These conditions are known to trigger apoptotic cell death in mammalian cells as a result of ischemia or anoxia. Anoxia-induced induction of apoptosis was investigated in four developmental stages of A . limnaeus that differ in their tolerance of anoxia, and thus may respond to anoxia uniquely. Exposure to staurosporine was used to determine if A . limnaeus cells were competent to enter apoptosis via cues other than anoxia. Apoptotic cells were identified by TUNEL assays and by measuring caspase 3/7 activity. Exposure to 48 hr of anoxia did not induce an increase in TUNEL-positive cells and generally did not lead to an increase in caspase 3/7 activity. However, treatment of anoxic embryos with 10 μM staurosporine resulted in a significant increase in caspase 3/7 activity in both normoxic and anoxic embryos. These results suggest that apoptosis is avoided in embryos of A . limnaeus following exposure to anoxia at least in part by mechanisms that prevent the activation of caspase 3/7 activity. While this mechanism remains unknown, it may be triggered by a protein kinase that can be experimentally inhibited by staurosporine.
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