Lung and Placenta Research Laboratory, Brigham Young University, Department of Physiology and Developmental Biology, Provo, UT, USA.
Lung and Placenta Research Laboratory, Brigham Young University, Department of Physiology and Developmental Biology, Provo, UT, USA.
Placenta. 2021 Jan 1;103:24-32. doi: 10.1016/j.placenta.2020.10.019. Epub 2020 Oct 15.
The Pyruvate kinase isozymes M2 (PKM2) protein is a metabolic enzyme that regulates the final step of glycolysis. This enzyme is present in highly proliferating cells and is expressed in the placenta. We recently demonstrated upregulated placental PKM2 during human intrauterine growth restriction (IUGR). Our current objective was to determine PKM2 regulation of trophoblast invasion, trophoblast PKM2 localization as well as mTOR protein expression, and to determine effects of activation of PKM2 during IUGR. Human placental tissues were obtained and analyzed by immunohistochemistry and western blot. Trophoblast cells were cultured in normoxic and hypoxic conditions and real time cell invasion and PKM2 protein were determined during activation (Fructose-6-bisphosphate; FBP6) or inhibition (Shikonin) of PKM2. In vivo studies determined the effects of PKM2 activation on placental and fetal weights. IUGR samples had elevated levels of p-PKM2. Different trophoblast PKM2 localization and expression was observed during normoxia and hypoxia. Decreased trophoblast invasion and PKM2 expression was observed during mTOR inhibition. Protection from decreased placental and fetal weights was observed by PKM2 activation. We conclude that PKM2 regulates trophoblast cell invasion depending on its subcellular location. Our results suggest that PKM2 regulation in trophoblast cells is more directly affected during hypoxia and its expression is regulated by mTOR activity. Additionally, we conclude that activation of PKM2 could reverse and/or rescue the deceased placental and fetal weights observed during IUGR. These results suggest that PKM2 could be a mediator of trophoblast cell invasion and its abundance influences the development of complicated pregnancies like IUGR.
丙酮酸激酶同工酶 M2 (PKM2) 蛋白是一种代谢酶,调节糖酵解的最后一步。这种酶存在于高度增殖的细胞中,并在胎盘组织中表达。我们最近发现,在人类宫内发育受限 (IUGR) 期间,胎盘组织中 PKM2 的表达上调。我们目前的目标是确定 PKM2 对滋养层细胞侵袭的调节作用、滋养层细胞 PKM2 的定位以及 mTOR 蛋白的表达,并确定在 IUGR 期间激活 PKM2 的作用。通过免疫组织化学和 Western blot 分析获得并分析了人胎盘组织。在常氧和低氧条件下培养滋养层细胞,并在激活(FBP6)或抑制(Shikonin)PKM2 时检测实时细胞侵袭和 PKM2 蛋白。体内研究确定了 PKM2 激活对胎盘和胎儿重量的影响。IUGR 样本中 p-PKM2 水平升高。在常氧和低氧条件下观察到不同的滋养层细胞 PKM2 定位和表达。在 mTOR 抑制时,观察到滋养层细胞侵袭和 PKM2 表达减少。通过 PKM2 激活,观察到对胎盘和胎儿重量减轻的保护作用。我们的结论是,PKM2 根据其亚细胞定位调节滋养层细胞的侵袭。我们的研究结果表明,在低氧条件下,PKM2 在滋养层细胞中的调节更直接受到影响,其表达受 mTOR 活性的调节。此外,我们的结论是,激活 PKM2 可以逆转和/或挽救 IUGR 期间观察到的胎盘和胎儿重量减轻。这些结果表明,PKM2 可能是滋养层细胞侵袭的介质,其丰度影响像 IUGR 这样复杂的妊娠的发育。