Department of Physiology, Shri BM Patil Medical College, Hospital & Research Centre, BLDE (Deemed to be University), Vijaypur, India.
Department of Physiology, SDM College of Medical Sciences & Hospital, Shri Dharmasthala Manjunatheshwara University, Dharwad, India.
J Basic Clin Physiol Pharmacol. 2021 Apr 21;33(4):419-428. doi: 10.1515/jbcpp-2020-0321.
Preeclampsia (PE) remains the major cause for maternal and foetal mortality and morbidity. Invasion of endovascular trophoblast and remodelling of spiral artery are crucial actions of normal placental development. Non-fulfilment of these processes plays a leading role in the development of preeclampsia. Vascular endothelial growth factor (VEGF) is produced by extravillous trophoblastic tissue and decidual cell population is a well-known angiogenic growth which plays a fundamental role in placental pathogenesis of PE. Annexin A2 (ANXA2) is a profibrinolytic protein receptor required for plasminolysis, which is an important step in the formation of new blood vessel along with VEGF. Role of ANXA2 is poorly studied in context with human reproductive disease like preeclampsia. The purpose of the present study is to examine the expression and association of VEGF and ANXA2 in the term placentas of pregnancies with and without PE.
The study group comprised of placental tissues procured from gestations with PE (n=30) and without (n=20) PE. The expression of VEGF and ANXA2 in the placental villous tissue was evaluated quantitatively by means of IHC, western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR).
Our IHC, western blotting and RT-PCR analysis illustrated the significant decrease in the expression of VEGF and ANXA2 in PE group compared with the normotensive control group (p<0.005). We observed statistically significant positive correlation among the expression of ANXA2 and VEGF in placentas of normotensive control group (p<0.0001).
The diminished expression of VEGF and ANXA2 in placenta may be associated with the defective angiogenesis and which may possibly play a vital role in PE pathogenesis.
子痫前期（PE）仍然是孕产妇和胎儿死亡和发病的主要原因。血管内滋养细胞浸润和螺旋动脉重塑是正常胎盘发育的关键步骤。这些过程的不满足在子痫前期的发展中起着主导作用。血管内皮生长因子（VEGF）由绒毛外滋养层组织产生，而蜕膜细胞群是一种众所周知的血管生成生长因子，在 PE 的胎盘发病机制中起着重要作用。膜联蛋白 A2（ANXA2）是纤维蛋白溶解蛋白受体，需要纤溶酶原激活，这是与 VEGF 一起形成新血管的重要步骤。ANXA2 在子痫前期等人类生殖疾病中的作用研究甚少。本研究旨在检查 VEGF 和 ANXA2 在有和没有 PE 的足月胎盘中的表达和相关性。
研究组包括来自患有 PE（n=30）和无 PE（n=20）妊娠的胎盘组织。通过免疫组织化学、Western blot 和逆转录-聚合酶链反应（RT-PCR）定量评估 VEGF 和 ANXA2 在胎盘绒毛组织中的表达。
我们的 IHC、Western blot 和 RT-PCR 分析表明，与正常血压对照组相比，PE 组中 VEGF 和 ANXA2 的表达显著降低（p<0.005）。我们观察到正常血压对照组胎盘组织中 ANXA2 和 VEGF 的表达之间存在统计学上显著的正相关（p<0.0001）。
胎盘中 VEGF 和 ANXA2 的表达减少可能与血管生成缺陷有关，这可能在 PE 的发病机制中发挥重要作用。
