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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inhibition of apoptosis in acute promyelocytic leukemia cells leads to increases in levels of oxidized protein and LMP2 immunoproteasome.
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Inhibition of apoptosis in acute promyelocytic leukemia cells leads to increases in levels of oxidized protein and LMP2 immunoproteasome.

机译：急性早幼粒细胞白血病细胞凋亡的抑制导致氧化蛋白和LMP2免疫蛋白酶体水平的增加。

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摘要

On reaching maturity, animal organs cease to increase in size because of inhibition of cell replication activities. It follows that maintenance of optimal organ function depends on the elimination of oxidatively damaged cells and their replacement with new cells. To examine the effects of oxidative stress and apoptosis on the accumulation of oxidized proteins, we exposed acute promyelocytic leukemia cells to arsenic trioxide (As(2)O(3)) in the presence and absence of a general caspase inhibitor (benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone), which is known to inhibit caspase-induced apoptosis. We confirm that treatment of cells with As(2)O(3) induces apoptosis and leads to the accumulation of oxidized proteins. Furthermore, inhibition of caspase activities prevented As(2)O(3)-induced apoptosis and led to a substantial increase in accumulation of oxidized proteins. Moreover, inhibition of caspase activity in the absence of As(2)O(3) led to elevated levels of the LMP2 immunoproteasome protein. We also show that caspase inhibition leads to increases in the levels of oxidized proteins obtained by treatments with hydrogen peroxide plus ferrous iron. Collectively, these results suggest the possibility that an age-related loss in capacity to carry out apoptosis might contribute to the observed accumulation of oxidized proteins during aging and in age-related diseases.
机译：达到成熟后，由于抑制细胞复制活性，动物器官的大小不再增加。因此，维持最佳器官功能取决于消除氧化损伤的细胞并用新细胞替代它们。若要检查氧化应激和凋亡对氧化蛋白积累的影响，我们在存在和不存在一般胱天蛋白酶抑制剂（苄氧羰基-Val-）的情况下，将急性早幼粒细胞白血病细胞暴露于三氧化二砷（As（2）O（3））。 Ala-Asp-氟甲基酮），已知可抑制caspase诱导的细胞凋亡。我们确认用As（2）O（3）处理细胞会诱导细胞凋亡并导致氧化蛋白的积累。此外，caspase活性的抑制阻止了As（2）O（3）诱导的细胞凋亡，并导致氧化蛋白积累的大量增加。此外，在没有As（2）O（3）的情况下抑制caspase活性导致LMP2免疫蛋白酶体蛋白水平升高。我们还表明，半胱天冬酶抑制导致通过用过氧化氢加亚铁处理的氧化蛋白水平增加。总的来说，这些结果表明年龄相关的执行凋亡能力的丧失可能有助于在衰老期间和与年龄相关的疾病中观察到氧化蛋白的积累。

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