Faculty Opinions recommendation of Effects of hypoxia-inducible factor-1alpha overexpression in pregnant mice: possible implications for preeclampsia and intrauterine growth restriction.

Gestational cholestasis is a common disease and is associated with adverse pregnancy outcomes. However, there are still no effective treatments. We investigated the effects of obeticholic acid (OCA) on fetal intrauterine growth restriction (IUGR) during 17α-ethynylestradiol- (E2-) induced gestational cholestasis in mice. All pregnant mice except controls were subcutaneously injected with E2 (0.625 mg/kg) daily from gestational day (GD) 13 to GD17. Some pregnant mice were orally administered with OCA (5 mg/kg) daily from GD12 to GD17. As expected, OCA activated placental, maternal, and fetal hepatic FXR signaling. Additionally, exposure with E2 during late pregnancy induced cholestasis, whereas OCA alleviated E2-induced cholestasis. Gestational cholestasis caused reduction of fetal weight and crown-rump length and elevated the incidence of IUGR. OCA decreased the incidence of IUGR during cholestasis. Interestingly, OCA attenuated reduction of blood sinusoid area in placental labyrinth layer and inhibited downregulation of placental sodium-coupled neutral amino acid transporter- (SNAT-) 2 during cholestasis. Additional experiment found that OCA attenuated glutathione depletion and lipid peroxidation in placenta and fetal liver and placental protein nitration during cholestasis. Moreover, OCA inhibited the upregulation of placental NADPH oxidase-4 and antioxidant genes during cholestasis. OCA activated antioxidant Nrf2 signaling during cholestasis. Overall, we demonstrated that OCA treatment protected against gestational cholestasis-induced placental dysfunction and IUGR through suppressing placental oxidative stress and maintaining bile acid homeostasis.

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Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function

Journal of the American Heart Association ◽

10.1161/jaha.117.005506 ◽

2017 ◽

Vol 6 (8) ◽

Cited By ~ 8

Author(s):

Maria Hennig ◽

Saskia Fiedler ◽

Christian Jux ◽

Ludwig Thierfelder ◽

Jörg‐Detlef Drenckhahn

Keyword(s):

Intrauterine Growth Restriction ◽

Growth Restriction ◽

Target Of Rapamycin ◽

Growth Morphology ◽

Cardiac Growth ◽

Rapamycin Treatment ◽

Intrauterine Growth ◽

Mechanistic Target Of Rapamycin ◽

Pregnant Mice ◽

And Function

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Arterial stiffness in women who subsequently developed isolated intrauterine growth restriction and preeclampsia

Ultraschall in der Medizin - European Journal of Ultrasound ◽

10.1055/s-0033-1354933 ◽

2013 ◽

Vol 34 (S 01) ◽

Author(s):

A Brückmann ◽

C Seeliger ◽

E Schleußner ◽

D Schlembach

Keyword(s):

Arterial Stiffness ◽

Intrauterine Growth Restriction ◽

Growth Restriction ◽

Intrauterine Growth

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Pathological features of the sequence in pregnant women with delayed fetal growth

HEALTH OF WOMAN ◽

10.15574/hw.2019.140.50 ◽

2019 ◽

pp. 50-54

Author(s):

V.O. Golyanovskiy ◽

◽

Ye.O. Didyk ◽

Keyword(s):

Pregnant Women ◽

Intrauterine Growth Restriction ◽

Normal Development ◽

Intrauterine Infection ◽

Normal Pregnancy ◽

Growth Restriction ◽

Control Group ◽

Intrauterine Growth ◽

Increased Risk ◽

Infection And Inflammation

Pregnant women with intrauterine growth restriction (IUGR) have an increased risk of adverse perinatal and long-term complications compared with the birth of children with normal body weight. Thus, IUGR is one of the main challenges for the global health system, especially in poor and developing countries. Morpho-functional studies of the placentas help in determining the causes of IUGR, and therefore, timely prevent complications in pregnant women with IUGR. The objective: The purpose of this study is to investigate various morphometric and pathomorphological changes in the placenta, including inflammatory, in cases of IUGR, and to establish a correlation of these results with the etiology and complications for the fetus. Materials and methods. In the current study, 54 placentas of the fetuses with IUGR (the main group) were compared with 50 placentas of the fetuses with normal development (control group). The criteria for the inclusion of IUGR were gestational age more than 30 weeks and all fetuses with a weight less than 10th percentile for this period of pregnancy. The placenta material was studied pathomorphologically with laboratory screening for infection and inflammation. Similarly, the results were determined for placentas of the fetuses with normal development compared to placentas with IUGR. Results. The placenta study showed the presence of calcification in the case of IUGR, as well as in the case of prolonged pregnancy. However, calcification of the placenta in the case of IUGR was more progressive compared with placenta in the normal pregnancy. In addition, the presence of intrauterine infection and inflammation was observed, which could also lead to an adverse outcome for the further progression of pregnancy with IUGR. Conclusion. A comparative macro- and microscopic pathomorphological study of the placentas in the two groups has shown a significant increase in the pathological changes in all the anatomical structures of the fetuses with IUGR. Key words: Intrauterine growth restriction (IUGR), fetal weight, pathomorphological changes of the placenta.

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