[doi: 10.5505/2017ichc.PP-100]
Immunolocalization of ANP and CNP in Healthy and Pre-Eclamptic Human Placental Tissue
Özlem Erekli̇1, Mustafa Öztop2, Kenan Çınar12Department of Biology, Mehmet Akif Ersoy University, Burdur, Turkey
Pre-eclampsia (PE), the leading cause of maternal and perinatal morbidity and mortality worldwide, affects 2-8% of all pregnancies worldwide. PE is characterized by the onset of hypertension from 20 weeks gestation and is associated with placental dysfunction and widespread maternal vascular endothelium. However, its underlying mechanism has remained elusive so far. C-type natriuretic peptide (CNP) is expressed in the decidua of the mouse placenta while atrial natriuretic peptide (ANP) expression has been demonstrated in the human placenta, especially in the cytotrophoblast tissue.
This study aimed to determine whether preeclampsia affects ANP and CNP expression in healthy and pre-eclamptic human placental tissues. The avidin-biotin complex was applied to 5 µm-thick formalin-fixed, paraffin-embedded human-placenta tissue sections mounted on poly-L-lysine–coated slides to demonstrate ANP and CNP immunoreactivity.
Immunostaining results reveal that weaker ANP and CNP immunoreactivity was in decidual cells of pre-eclamptic individuals. Cytotrophoblast cells had more intense immunoreactivity to ANP and CNP in the preeclampsia. Some blood cells showed immunostaining with ANP and CNP in both preeclampsia and control group. There were ANP and CNP staining in the atheromatous plaques seen in the vessels of preeclamptic patients. Intense immunostaining was observed in extravillous trophoblasts without any significant difference between both groups in terms of staining intensity. Weaker ANP and CNP staining were seen in the chorionic fetal vessels of the control group than of the preeclampsia.
Altered synthesis or action of autocrine or paracrine vasoactive factors such as ANP and CNP in endothelial or vascular smooth muscle cells may mediate changes in vascular resistance in pregnancy. When patients with pre-eclampsia develop hypertension, it may lead to an increase in the synthesis of ANP and CNP synthesized by chorionic vessels. This may act as a compensatory mechanism, thus preventing the fetus from being affected by the preeclampsia. Yet, results from different studies appear to be inconsistent. Our study has also several limitations such as the low number of patients and lack of biochemical data. It is, therefore, difficult to draw firm conclusions from the results, and further studies are needed which will examine a large group of samples.
ANP-control
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ANP-preeclampsia
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CNP-control
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CNP-preeclampsia
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