Abstract
Disregarding the multiple research in the field of preeclampsia, the exact pathology remains unclear. The shallow invasion of extravillous trophoblast (EVT) in spiral arteries leads to the development of pregnancy‐induced hypertension, nevertheless the etiological factor is unknown. Disturbed differentiation of EVT and incorrect placental angiogenesis seem to be one of the most important starting points for pathogenetic and etiological concepts in preeclampsia. As fractalkine (chemokine CX3CL1) by the activation of its only receptor CX3CR1 stimulates angiogenesis and integrin‐dependent cell migration, the authors ask the question about the possible role of CX3CL1 in placental angiogenesis in preeclampsia. A total number of 58 pregnant patients were included into the study, preeclampsia was diagnosed in 29 patients, and 29 patients were healthy, normotensive term pregnancies. In all women between 30 and 32 week of pregnancy CX3CL1 level was assessed in plasma using ELISA and the expression of CX3CR1 and angiogenesis score (V/EVTI: vascular/extravascular tissular index) were assessed in placental tissues obtained after delivery. Quantitative immunohistochemistry was applied for assessment of both CX3CR1 expression and V/EVTI in placental sections. For this second purpose, morphometric measurements of the placental microvasculature were performed after immunohistochemistry of endothelial cells with CD‐34 antibody. The average duration of pregnancy in preeclamptic group was shorter by 5,3 weeks than in normotensive pregnancies. CXC3CL1 plasma concentration was significantly lower in preeclamptic patients (mean 279 pg/ml ± 243 vs mean 846 pg/ml ± 418), whereas CX3CR1 expression was significantly (p < 0.05) higher in preeclamptic group. A negative correlation between CX3CL1 level and CX3CR1 expression was observed. Moreover, the V/EVTI value was lowered in preeclampsia (p < 0.05). In conclusion, disturbed placental angiogenesis in preeclampsia may be associated with low plasma fractalkine level.Support or Funding InformationWUM grant: 2M2‐W1‐18This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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