Platelets in Fetal Growth Restriction: Role of Reactive Oxygen Species, Oxygen Metabolism, and Aggregation.
Joanna NowaczykBarbara PoniedziałekPiotr RzymskiDominika SikoraMariola Ropacka-LesiakPublished in: Cells (2022)
Fetal growth restriction (FGR) is mainly caused by failure of the uteroplacental unit. The exact pathogenesis remains unclear. The cause is thought to be related to abnormal platelet activation, which may result in microthrombus formation in the small vessels of the placenta. Reactive oxygen species (ROS) may initiate the pathological process of platelet activation. This study aimed to evaluate selected platelet parameters in pregnancy complicated by FGR and relate them to the severity of hemodynamic abnormalities. A total of 135 women (pregnant with FGR, with an uncomplicated pregnancy, and non-pregnant) were enrolled to study different platelet parameters: count (PLT), mean volume (MPV), ROS levels, intracellular oxygen level, oxygen consumption, and aggregation indices. No abnormalities in PLT and MPV were found in the FGR group, although it revealed increased ROS levels in platelets, lower platelet oxygen consumption, and intraplatelet deprivation. Aggregation parameters were similar as in uncomplicated pregnancy. No significant relationships were observed between hemodynamic abnormalities and the studied parameters. Platelets in pregnancies complicated by FGR may reveal an impaired oxidative metabolism, which may, in turn, lead to oxidative stress and, consequently, to an impaired platelet function. This study adds to the understanding of the role of platelets in the etiology of FGR.
Keyphrases
- reactive oxygen species
- preterm birth
- pregnancy outcomes
- dna damage
- cell death
- type diabetes
- metabolic syndrome
- gene expression
- single cell
- adipose tissue
- insulin resistance
- skeletal muscle
- red blood cell
- molecular dynamics
- sensitive detection
- ischemia reperfusion injury
- urinary tract infection
- endoplasmic reticulum stress
- density functional theory