McCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB T2N 1N4, Canada.
Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 1N4, Canada.
Cells. 2022 Apr 7;11(8):1256. doi: 10.3390/cells11081256.
Platelets may be pivotal mediators of the thrombotic and coagulopathic complications of preeclampsia (PE), linking inflammation and thrombosis with endothelial and vascular dysfunction. Both PE and gestational hypertension (GH) fall within the spectrum of hypertensive complications of pregnancy, with GH being a risk factor for preeclampsia. However, it is unclear what biomarkers distinguish PE from GH. Using a discovery size cohort, we aimed to characterize specific plasma and platelet thrombo-inflammatory drivers indicative of PE and differentiate PE from GH. We performed multiplex immunoassays, platelet and plasma quantitative proteomics and metabolomics of PE patients, comparing with non-pregnant (NP), healthy pregnant controls (PC) and GH participants. The expression pattern of plasma proteins and metabolites in PE/GH platelets was distinct from that of NP and PC. Whilst procoagulation in PC may be fibrinogen driven, inter-alpha-trypsin inhibitors ITIH2 and ITIH3 are likely mediators of thrombo-inflammation in GH and PE, and fibronectin and S100A8/9 may be major procoagulant agonists in PE only. Also enriched in PE were CCL1 and CCL27 plasma cytokines, and the platelet leucine-rich repeat-containing protein 27 and 42 (LRRC27/42), whose effects on platelets were explored using STRING analysis. Through protein-protein interactions analysis, we generated a new hypothesis for platelets' contribution to the thrombo-inflammatory states of preeclampsia.
血小板可能是子痫前期(PE)血栓形成和凝血异常并发症的关键介质,将炎症和血栓形成与内皮和血管功能障碍联系起来。PE 和妊娠高血压(GH)都属于妊娠高血压并发症的范畴,GH 是 PE 的一个危险因素。然而,目前尚不清楚哪些生物标志物可以将 PE 与 GH 区分开来。本研究使用发现队列,旨在描述特定的血浆和血小板血栓炎症驱动因素,以指示 PE,并将 PE 与 GH 区分开来。我们对 PE 患者进行了多重免疫分析、血小板和血浆定量蛋白质组学和代谢组学分析,与非妊娠(NP)、健康妊娠对照组(PC)和 GH 参与者进行了比较。PE/GH 血小板中的血浆蛋白和代谢物的表达模式与 NP 和 PC 不同。虽然 PC 中的促凝作用可能由纤维蛋白原驱动,但抗胰蛋白酶抑制剂 ITIH2 和 ITIH3 可能是 GH 和 PE 中血栓炎症的介导物,纤维连接蛋白和 S100A8/9 可能是仅在 PE 中起主要促凝作用的激动剂。PE 中还富含 CCL1 和 CCL27 等血浆细胞因子,以及血小板富含亮氨酸重复蛋白 27 和 42(LRRC27/42),使用 STRING 分析探讨了它们对血小板的影响。通过蛋白质-蛋白质相互作用分析,我们提出了一个新的假设,即血小板可能参与了子痫前期的血栓炎症状态。