Li Lianqin, Shoji Wataru, Oshima Hiroaki, Obinata Masuo, Fukumoto Manabu, Kanno Naoko
Department of Cell Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575, Japan.
FEBS Lett. 2008 Jul 9;582(16):2431-4. doi: 10.1016/j.febslet.2008.05.050. Epub 2008 Jun 9.
We observed frequent stillbirth in peroxiredoxin III (PrxIII) knockout maternal mice. Quantitative real time PCR (qRT-PCR) and Western-blot analysis revealed increased oxidative stress in placentas that were deficient in PrxIII. We did not find significant difference between PrxIII knockout maternal mice and wild-type littermates in hematological parameters, fetal number, and embryonic development. Nevertheless, we noticed enhanced expression of PrxI in erythrocytes of pregnant knockout mice. Our results provided in vivo evidence that PrxIII played a crucial role in placental antioxidant defense. Up-regulation of PrxI might provide a compensation that protected erythrocytes against oxidative damage.
我们观察到过氧化物酶III（PrxIII）基因敲除的母鼠频繁出现死产。定量实时PCR（qRT-PCR）和蛋白质免疫印迹分析显示，PrxIII缺乏的胎盘氧化应激增加。在血液学参数、胎儿数量和胚胎发育方面，我们未发现PrxIII基因敲除的母鼠与其野生型同窝仔鼠之间存在显著差异。然而，我们注意到怀孕的基因敲除小鼠红细胞中PrxI的表达增强。我们的结果提供了体内证据，表明PrxIII在胎盘抗氧化防御中起关键作用。PrxI的上调可能提供一种补偿作用，保护红细胞免受氧化损伤。
