Placental ultrastructural and immunohistochemical changes in preeclampsia with concomitant fetal growth restriction


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Abstract

Aim. To investigate the ultrastructural and immunohistochemical changes occurring in the placenta in preeclampsia (PE) with concomitant fetal growth restriction (FGR). Materials and methods. The study comprised 33patients who underwent operative delivery. Among them, 15 and 8 women had severe and moderate PE, respectively. The control group included 10 women with an uncomplicated full-term pregnancy. Six women with severe PE had FGR. A histological examination of hematoxylin-eosin stained sections was performed along with immunohistochemical studies using primary polyclonal antibodies to TLR8 (1: 250; GenTex). Besides, 10 placental specimens were examined using a Philips CM 100 transmission electron microscope (Philips/FEI Corporation, Eindhoven, Holland). Results. In patients with severe PE, the findings of electron microscopy showed damage to membranes with a reduction of microvilli on the surface of syncytiotrophoblast (SCT), cytoplasm vacuolization, damage to membranes and apical parts of cells. In patients with moderate PE, microvilli remained on the SCT surface. A characteristic change in the SCT ultrastructure in moderate PE was the appearance in the cytoplasm of numerous vacuoles of different sizes formed by swelling and dilatation of cisterns of granular endoplasmic reticulum. The findings of immunohistochemical studies demonstrated that membrane and cytoplasmic TLR8 staining of SCT and syncytial knots (SK) was most pronounced in PE with concomitant FGR and the least in uncomplicated physiological pregnancy (p<0.01). Besides, in moderate PE, membrane staining in SCT and SK was predominant, while severe PE was associated with mainly cytoplasmic staining (p <0.01). Conclusion. Severe PE is associated with damage to SCT membranes, which disrupts the placental barrier resulting in placental insufficiency. Patients with severe PE have over-expression of TLR8 in SCT. It cannot be ruled out that FGR is caused by the activation of inflammatory cascades resulting from over-expression of TLR8 and the high pro-inflammatory response of trophoblast.

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About the authors

N. V Nizyaeva

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: niziaeva@gmail.com

E. Yu Amiraslanov

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: e_amiraslanov@oparina4.ru

N. A Lomova

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: natasha-lomova@yandex.ru

S. V Pavlovich

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: s_pavlovich@oparina.ru

N. A Savel’eva

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

M. N Nagovitsyna

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: moremore84@mail.ru

T. V Sukhacheva

A.N. Bakulev Scientific Center of Cardiovascular Surgery of Minzdrav of Russia

Email: tatiana@box.ru

R. A Serov

A.N. Bakulev Scientific Center of Cardiovascular Surgery of Minzdrav of Russia

A. I Shchegolev

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: ashegolev@oparina4.ru

N. E Kan

V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology of Minzdrav of Russia

Email: kan-med@mail.ru

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