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首页> 美国卫生研究院文献>Biology of Reproduction >Elevated Levels of Uterine Anti-Apoptotic Signaling May Activate NFKB and Potentially Confer Resistance to Caspase 3-Mediated Apoptotic Cell Death During Pregnancy in Mice
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Elevated Levels of Uterine Anti-Apoptotic Signaling May Activate NFKB and Potentially Confer Resistance to Caspase 3-Mediated Apoptotic Cell Death During Pregnancy in Mice

机译：子宫抗凋亡信号水平升高可能会激活NFKB并可能在小鼠妊娠期间对Caspase 3介导的凋亡细胞死亡产生抗性。

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Preserving the uterus in a state of relative quiescence is vital to the maintenance of a successful pregnancy. Elevated cytoplasmic levels of uterine caspase 3 during pregnancy have been proposed as a potential regulator of uterine quiescence through direct targeting and disabling of the uterine contractile architecture. However, despite highly elevated levels of uterine caspase 3 during pregnancy, there is minimal evidence of apoptosis. This current study defines the mechanism whereby the pregnant uterine myocyte may harness the tocolytic activity of active caspases while avoiding apoptotic cell death. Using the pregnant mouse model, we have analyzed the uterus for changes in pro- and antiapoptotic signaling patterns associated with the advancing stages of pregnancy. Briefly, we have found that members of the IAP family, such as SURVIVIN and XIAP, and the Bcl2 family members, such as MCL1, are elevated in the uterine myocyte during late gestation. The IAP family members are the only endogenous inhibitors of active caspase 3, and MCL1 limits activation of caspase 3 by suppressing proapoptotic signaling. Elevated XIAP levels partner with SURVIVIN, resulting in increased levels of the antiapoptotic MCL1 via NFKB activation; these together have the potential to limit both the activity and level of active caspase 3 in the pregnant uterus as term approaches. We propose that modification of these antiapoptotic signaling partners allows the pregnant uterus to escape the apoptotic action of elevated active caspase 3 levels but also functions to limit the levels of active uterine caspase 3 near term.
机译：将子宫保持在相对静止的状态对于维持成功的怀孕至关重要。已经提出，通过直接靶向和使子宫收缩结构失能，在怀孕期间子宫胱天蛋白酶3的细胞质水平升高是子宫静止的潜在调节剂。然而，尽管在怀孕期间子宫caspase 3的水平非常高，但几乎没有凋亡迹象。这项当前的研究定义了一种机制，通过这种机制，怀孕的子宫肌细胞可以利用活性胱天蛋白酶的溶卵活性，同时避免凋亡性细胞死亡。使用怀孕的小鼠模型，我们分析了子宫中与妊娠进展阶段相关的促凋亡和抗凋亡信号传导模式的变化。简而言之，我们发现IAP家族的成员（例如SURVIVIN和XIAP）和Bcl2家族的成员（例如MCL1）在妊娠后期的子宫肌细胞中升高。 IAP家族成员是活性胱天蛋白酶3的唯一内源性抑制剂，而MCL1通过抑制凋亡信号传导来限制胱天蛋白酶3的激活。 XIAP水平升高与SURVIVIN结合，通过NFKB激活导致抗凋亡MCL1水平升高；随着期限的临近，这些都可能限制孕妇子宫中活性胱天蛋白酶3的活性和水平。我们建议这些抗细胞凋亡信号伴侣的修改允许怀孕的子宫逃脱升高的活性胱天蛋白酶3水平的凋亡作用，但也具有限制活性子宫胱天蛋白酶3短期水平的作用。

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