Relationship between elevated lipid peroxides,vitamin E deficiency and hypertension in preeclampsia

Preeclampsia or pregnancy-induced hypertension is a major cause of both maternal and fetal-neonatal morbidity and mortality. The deficiency of vitamin E can cause accumulation of lipid peroxidation products, which, in turn, can induce vasoconstriction. This study has examined any evidence of increased cellular lipid peroxidation and accumulation of malonydialdehyde (MDA, an end product of lipid peroxidation) in pregnancy-induced hypertension and any relationship between the elevated MDA and lower vitamin E levels with hypertension in pregnant women. EDTA-Blood was collected from pregnant women at the time of delivery. Plasma vitamin E was determined by HPLC; MDA by the thiobarbituric acid-reactivity. Subjects with diastolic blood pressure(DBP) 90 mm Hg were considered hypertensive (HT) and with <90 mm Hg normotensive (NT). Data (Mean±SE) from 49 NT and 11 HT women show that HT has significantly lower vitamin E (22±1 vs 27±1 nmole/ml, p<0.03) and elevated MDA levels (0.56±0.06 vs 0.43±0.02 nmole/ml, p<0.03) compared to NT; the ages and gestational ages of women were similar. Among all women, there was a significant positive relationship between DBP and MDA levels (r=0.27, p<0.05), and a significant negative relationship between vitamin E levels and DBP (–0.36, p<0.005), and a significant negative relationship between MDA and vitamin E levels (r=–0.27, p<0.05). Thus, HT women's plasma has significantly lower E and higher MDA levels, and DBP significantly correlates with the extent of vitamin E deficiency and increased MDA levels. This study suggests a relationship between elevated lipid peroxidation and lower vitamin E levels and hypertension in pregnancy (preeclampsia).     

Vitamin D and maternal and child health: Overview and implications for dietary requirements

The essentiality of vitamin D for normal growth and development has been recognized for over 80 years, and vitamin D fortification programs have been in place in the United States for more than 70 years. Despite the above, vitamin D deficiency continues to be a common finding in certain population groups. Vitamin D deficiency has been suggested as a potential risk factor for the development of preeclampsia, and vitamin D deficiency during infancy and early childhood is associated with an increased risk for numerous skeletal disorders, as well as immunological and vascular abnormalities. Vitamin D deficiency can occur through multiple mechanisms including the consumption of diets low in this vitamin and inadequate exposure to environmental ultraviolet B rays. The potential value of vitamin D supplementation in high‐risk pregnancies and during infancy and early childhood is discussed. Currently, there is vigorous debate concerning what constitutes appropriate vitamin D intakes during early development as exemplified by differing recommendations from the Institute of Medicine Dietary Reference Intake report and recent recommendations by the Endocrine Society. As is discussed, a major issue that needs to be resolved is what key biological endpoint should be used when making vitamin D recommendations for the pregnant woman and her offspring. Birth Defects Research (Part C) 99:24–44, 2013. © 2013 Wiley Periodicals, Inc.     

Function and control of human invasive trophoblast subtypes: Intrinsic vs. maternal control

ABSTRACT

The establishment of a functional placenta is pivotal for normal fetal development and the maintenance of pregnancy. In the course of early placentation, trophoblast precursors differentiate into highly invasive trophoblast subtypes. These cells, referred to as extravillous trophoblasts (EVTs), penetrate the maternal uterus reaching as far as the inner third of the myometrium. One of the most fundamental functions of EVTs is the transformation of spiral arteries to establish the uteroplacental blood circulation assuring an adequate nutrient and gas supply to the developing fetus. To achieve this, specialized EVT subpopulations interact with maternal immune cells, provoke elastolysis in the arterial wall and replace the endothelial cells lining the spiral arteries to induce intraluminal vascular remodeling. These and other trophoblast-mediated processes are tightly controlled by paracrine signals from the maternal decidua and furthermore underlie an intrinsic cell-type specific program. Various severe pregnancy complications such as preeclampsia or intrauterine growth retardation are associated with abnormal EVT function, shallow invasion, and decreased blood flow to the placenta. Hence a better understanding of human trophoblast invasion seems mandatory to improve therapeutic intervention. This approach, however, requires a profound knowledge of the human placenta, its various trophoblast subtypes and in particular a better understanding of the regulatory network that controls the invasive phenotype of EVTs.     

Toll-like receptors signaling network in pre-eclampsia: An updated review

Toll-like receptors (TLRs) are innate immune cells receptors. They are expressed on leukocytes, epithelial cells, and more particularly on placental immune cells and chorion trophoblast. Upregulation of innate immune response occurs during normal pregnancy, but its excessive activity is involved in the pathology of pregnancy complications including pregnancy-induced hypertension and pre-eclampsia (PE). The recent studies about the overmuch inflammatory responses and aberrant placentation are associated with increased expression of TLRs in PE patients. This review has tried to focus on the relationship between some activities of TLRs and the risk of preeclampsia development.     

低分子肝素对早发型重度子痫前期治疗对母婴结局的影响分析

目的:探讨低分子肝素对早发型重度子痫前期治疗情况,并分析治疗对母婴结局的影响。方法:选择我院2012年1月~12月收治的早发型重度子痫前期患者120例,随机分为观察组和对照组,每组60例。对照组给予常规治疗,观察组在对照组治疗基础上加用低分子肝素。比较两组血压、24 h尿量、尿蛋白定量、尿酸、血常规、凝血功能及孕周延长时间、围产儿结局和产妇并发症。结果:两组患者临床指标无差异(P0.05),治疗后两组血压、24 h尿量、尿蛋白定量均显著改善,观察组红细胞压积、纤维蛋白原降低明显高于对照组,而观察组患者的产妇并发症和围产儿不良结局发生率均低于对照组,且产妇孕周延长时间明显多于对照组,差异有统计学意义(P0.05)。两组患者的血小板、凝血酶原时间等治疗前后均无明显变化(P0.05)。结论:低分子肝素对早发型重度子痫前期的治疗能有效抑制高凝状态,改善肾功能,延长孕周时间,可有效减少患者并发症的发生,改善母婴预后,值得临床推广应用。     

Trophoblast–endothelium signaling involves angiogenesis and apoptosis in a dynamic bioprinted placenta model

Trophoblast invasion and remodeling of the maternal spiral arteries are required for pregnancy success. Aberrant endothelium–trophoblast crosstalk may lead to preeclampsia, a pregnancy complication that has serious effects on both the mother and the baby. However, our understanding of the mechanisms involved in this pathology remains elementary because the current in vitro models cannot describe trophoblast–endothelium interactions under dynamic culture. In this study, we developed a dynamic three-dimensional (3D) placenta model by bioprinting trophoblasts and an endothelialized lumen in a perfusion bioreactor. We found the 3D printed perfusion bioreactor system significantly augmented responses of endothelial cells by encouraging network formations and expressions of angiogenic markers, cluster of differentiation 31 (CD31), matrix metalloproteinase-2 (MMP2), matrix metalloproteinase-9 (MMP9), and vascular endothelial growth factor A (VEGFA). Bioprinting favored colocalization of trophoblasts with endothelial cells, similar to in vivo observations. Additional analysis revealed that trophoblasts reduced the angiogenic responses by reducing network formation and motility rates while inducing apoptosis of endothelial cells. Moreover, the presence of endothelial cells appeared to inhibit trophoblast invasion rates. These results clearly demonstrated the utility and potential of bioprinting and perfusion bioreactor system to model trophoblast–endothelium interactions in vitro. Our bioprinted placenta model represents a crucial step to develop advanced research approach that will expand our understanding and treatment options of preeclampsia and other pregnancy-related pathologies.     

Haemodynamics using transthoracic echocardiography in healthy pregnant and non-pregnant baboons (Papio hamadryas)

Background To determine systolic and diastolic function using transthoracic echocardiography in the baboon (Papio hamadryas). Methods Transthoracic echocardiography was performed in eight non‐pregnant female and six pregnant baboons according to American Society of Echocardiography recommendations. Results Haemodynamic measurements were obtained from fourteen baboons. Compared to non‐pregnant baboons, pregnant baboons demonstrated: (mean ± SD, pregnant vs. healthy) increased cardiac output (1615 ± 121 ml/minutes vs. 1317 ± 134 ml/minutes P = 0.001) due to an increased heart rate [120 ± 11 beats per minute (BPM) vs. 105 ± 6 BPM P = 0.018]. The inter‐observer and intra‐observer variability (mean difference ± SD) for the left ventricular outflow tract diameter was 0.05 ± 0.07 cm and 0.01 ± 0.03 cm respectively. There was minimal impact to the animal’s daily activities. Conclusions Transthoracic echocardiography was applicable and reproducible for the assessment of haemodynamics in baboons thus enabling translation of animal results to human studies.