Cotyledon and binucleate cell nitric oxide synthase expression in an ovine model of fetal growth restriction
Cotyledon and binucleate cell nitric oxide synthase expression in an ovine model of fetal growth restriction
复制标题
DOI：
10.1152/jappl.2001.90.6.2420
复制
发表时间：
2001-06-01
影响因子：
3.3
通讯作者：
Abman, SH
中科院分区：
文献类型：
--
作者：
Galan, HL;Regnault, TRH;Abman, SH
绵羊妊娠早期的热暴露导致胎盘功能不全和宫内生长受限（PI-IUGR）。我们假设，在这个模型中，热暴露破坏胎盘结构，减少胎盘内皮型一氧化氮合酶（eNOS）蛋白的表达。我们测量了eNOS蛋白含量，并进行了eNOS的免疫组织化学从热中性（TN）和高温（HT）的动物在妊娠中期（90天）被杀的胎盘。比较各组胎盘组织形态计量学。与TN对照组相比，HT组显示分娩重量减少（457 +/- 49 vs. 631 +/- 21 g; P< 0.05）和胎盘重量减少的趋势（288 +/- 61 vs. 554 +/- 122 g; P = 0.09）。HT组子叶eNOS蛋白含量较对照组减少50%（P< 0.03）。eNOS定位于两个实验组的滋养层内的血管内皮细胞和双核细胞（BNC）相似。HT子叶显示胎儿与母体基质组织的比率降低（1.36 +/- 0.36 vs. 3.59 +/- 1.2; P小于或等于0.03）。我们的结论是，eNOS蛋白表达减少，在这个模型的PI-IUGR和eNOS定位于血管内皮细胞和BNC。我们推测，在PI-IUGR模型中，正常血管发育和BNC eNOS产生和功能的破坏导致胎盘血管张力和血流异常。
Heat exposure early in ovine pregnancy results in placental insufficiency and intrauterine growth restriction (PI-IUGR). We hypothesized that heat exposure in this model disrupts placental structure and reduces placental endothelial nitric oxide synthase (eNOS) protein expression. We measured eNOS protein content and performed immunohistochemistry for eNOS in placentas from thermoneutral (TN) and hyperthermic (HT) animals killed at midgestation (90 days). Placental histomorphometry was compared between groups. Compared with the TN controls, the HT group showed reduced delivery weights (457 +/- 49 vs. 631 +/- 21 g; P< 0.05) and a trend for reduced placentome weights (288 +/- 61 vs. 554 +/- 122 g; P = 0.09). Cotyledon eNOS protein content was reduced by 50% in the HT group (P< 0.03). eNOS localized similarly to the vascular endothelium and binucleated cells (BNCs) within the trophoblast of both experimental groups. HT cotyledons showed a reduction in the ratio of fetal to maternal stromal tissue (1.36 +/- 0.36 vs. 3.59 +/- 1.2; P less than or equal to 0.03). We conclude that eNOS protein expression is reduced in this model of PI-IUGR and that eNOS localizes to both vascular endothelium and the BNC. We speculate that disruption of normal vascular development and BNC eNOS production and function leads to abnormal placental vascular tone and blood flow in this model of PI-IUGR.