Platelets in Preeclampsia: Function and Role in the Inflammation

Abstract

Preeklampside trombositlerin enflamasyondaki rolü ve etkileriPreeklampsi tüm gebeliklerin %5-8' ini komplike eden gebeliğin hipertansif hastalığıdır. Preeklampsi patogenezinde kılcal damar yatağındaki inflamasyon önemli rol oynar. Preeklampside olduğu gibi dolaşımda serbest halde bulunan mikropartiküllerle trombositlerin karşılaşması sonucunda trombositler aktive olurlar. Aktive olan trombositler dolaşıma serbest moleküller salarlar ve hücre yüzeylerindeki adhezyon moleküllerinin artmasına neden olurlar. Serbest moleküller trombosit, lökosit ve endotel hücreleri arasındaki etkileşimleri düzenlerler. Adhezyon molekülleri de trombosit, lökosit ve endotel hücrelerinin birbirlerine bağlanmasına aracılık ederler. Oluşan trombosit-lökosit agregatları nötrofillerin inflamasyonun olduğu damarsal yapılara göçünün artmasına neden olur. Ayrıca, endotel hücrelerine bağlanan trombositler sitokinlerin yapımına ve inflamatuvar yanıtın artmasına neden olur. Bu derlemede, preeklamptik gebelerde trombosit fonksiyon bozuklukları ve trombositlerin preeklampsi patogenezindeki inflamatuvar rolünden bahsedeceğiz. Anahtar sözcükler: Preeklampsi, trombosit aggregasyonu, trombosit aktivasyonu, inflamasyon ABS TRACT Platelets in preeclampsia: function and role in the inflammationPreeclampsia is a hypertensive disease of pregnancy complicating 5-8% of all pregnancies. A growing body of evidence demonstrated that inflammation in microvasculature plays a major role in the pathogenesis of preeclampsia. Although circulating platelets are in rested state, when they are exposed to soluble mediators or microparticles in the inflamed vasculature as in preeclampsia, platelets are activated by engagement of the mediators on surface receptors. Upon activation, platelets degranulate some soluble and adhesion molecules. When soluble mediators released into the local microenvironment, they modulate the interactions between platelets, leukocytes and endothelial cells. Adhesion molecules expressed on the surface may initiate adherence between platelets, leukocytes and endothelial cells. Platelet-leukocyte aggregates promote the recruitment of neutrophils into the inflamed microvasculature. In addition to this, adherent platelets on endothelial cells induce production of inflammatory cytokines thus lead to amplification of inflammatory response. In this review, we mention platelet dysfunction in preeclamptic pregnancies and inflammatory role of platelets in the pathogenesis of preeclampsia.

Correlation of platelet parameters with adverse maternal and neonatal outcomes in severe preeclampsia: A case-control study

“…Enhanced thrombopoiesis produces younger and larger platelets that are metabolically and enzymatically more active [ 12 , 13 ]. The inflammatory response is intensified in pre-eclampsia by the induction of inflammatory cytokines by adherent platelets on endothelial cells culminating in severe hemostatic, vascular, and coagulation abnormalities that cause serious feto-maternal complications [ 17 ].…”

Angiogenesis, Lymphangiogenesis, and the Immune Response in South African Preeclamptic Women Receiving HAART

“…Vascular development is influenced by PECAM-1 through the formation of a complex with VEGFR-2 and VE cadherin [35]. In PE, PECAM-1 induces neutrophil and platelet activation, thereby promoting vascular damage [36]. Thakoordeen et al (2017) demonstrated a similar level of PECAM-1 between control and preeclamptic pregnancies ( p = 0.07), while no correlation was found based on HIV infection ( p = 0.68) or across study groups ( p = 0.24) [37].…”

Differences of Main Levels of Serum P-Selectin and Trombosite in Severe Preeclampsia and Eclampsia

“…Healthy vascular endothelium secretes several mediators such as nitric oxide (NO), and adenosine which inhibits platelet activation, adhesion to endothelium. 2,13 However, inflammation of the endothelium results in the production of these protective mediators being reduced. NO and adenosine metabolites are increased in pre-eclampsia patients in parallel to significant platelet activation compared with normotensive pregnancies.10 Lyall et al demonstrated that NO concentrations are increased in the feto-placental circulation in preeclampsia.…”

“…They also suggest that elevated NO levels further complement platelet activation in preeclamptic women. 13 Circulating platelets are exposed to soluble factors such as lipid mediators, cytokines, and chemokines which are released by activated leukocytes and endothelial cells due to inflammation of the blood vessels. The accumulation of these mediators gives rise to an activation response characterized by degra-nulation of platelet granules.…”