PDF(Pubmed)
Abstract：
Placental protein 13 (PP13) exhibits a plasma concentration that increases gradually during normal gestation, a process that is disrupted in preeclampsia, which is characterized by elevated vascular resistance, reduced utero-placental blood flow, and intrauterine growth restriction. This study investigated PP13\'s role in vascular tone regulation and its molecular mechanisms. Uterine and subcutaneous arteries, isolated from both pregnant and non-pregnant women, were precontracted with the thromboxane analogue U46619 and exposed to PP13 using pressurized myography. The molecular mechanisms were further investigated, using specific inhibitors for nitric oxide synthase (L-NAME+LNNA at 10-4 M) and guanylate cyclase (ODQ at 10-5 M). The results showed that PP13 induced vasodilation in uterine arteries, but not in subcutaneous arteries. Additionally, PP13 counteracted U46619-induced vasoconstriction, which is particularly pronounced in pregnancy. Further investigation revealed that PP13\'s mechanism of action is dependent on the activation of the nitric oxide-cGMP pathway. This study provides novel insights into the vasomodulatory effects of PP13 on human uterine arteries, underscoring its potential role in regulating utero-placental blood flow. These findings suggest that PP13 may be a promising candidate for improving utero-placental blood flow in conditions such as preeclampsia. Further research and clinical studies are warranted to validate PP13\'s efficacy and safety as a therapeutic agent for managing preeclampsia.
摘要：
胎盘蛋白13（PP13）的血浆浓度在正常妊娠期间逐渐增加，先兆子痫中断的过程，其特征是血管阻力升高，子宫胎盘血流量减少，和宫内生长受限.本研究探讨了PP13在血管张力调节中的作用及其分子机制。子宫和皮下动脉，与孕妇和非孕妇隔离，使用血栓烷类似物U46619预收缩，并使用加压肌电图暴露于PP13。进一步研究了分子机制,使用一氧化氮合酶（10-4M的L-NAMELNNA）和鸟苷酸环化酶（10-5M的ODQ）的特异性抑制剂。结果显示PP13诱导子宫动脉血管舒张,但不是皮下动脉.此外,PP13抵消了U46619诱导的血管收缩，这在怀孕期间尤为明显。进一步的研究表明，PP13的作用机制依赖于一氧化氮-cGMP途径的激活。这项研究为PP13对人子宫动脉的血管调节作用提供了新的见解，强调其在调节子宫胎盘血流量方面的潜在作用。这些发现表明，PP13可能是在先兆子痫等情况下改善子宫胎盘血流量的有希望的候选者。需要进一步的研究和临床研究来验证PP13作为治疗先兆子痫的治疗药物的有效性和安全性。
