Morphological Changes of the Spiral Arteries in the Placentae Bed in Relation to Pre‐eclampsia and Fetal Growth Retardation

Gerretsen, G.; Huisjes, H.J.; Elema, Jd

doi:10.1111/j.1471-0528.1981.tb02222.x

Cited by 347 publications

(154 citation statements)

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“…The blood vessel walls are remodeled by this invasion at the maternal-fetal interface to provide sufficient nutrients and oxygen for the fetus [3,4]. Impaired invasion of trophoblast cells into the maternal tissue or insufficient uterine spiral artery remodeling may lead to preeclampsia (PE) [2,5], intrauterine growth restriction [6] and other obstetric complications [7,8]. The detailed molecular mechanism involved in regulating trophoblast invasion requires further elucidation.…”

Section: Introductionmentioning

confidence: 99%

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

et al. 2015

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Section: Introductionmentioning

confidence: 99%

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

et al. 2015

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“…During normal placental development, cytotrophoblasts invade the maternal spiral arterioles and completely remodel the maternal spiral arterioles into large capacitance vessels with low resistance (12). This endovascular cytotrophoblast invasion involves replacement of not only the endothelium but also the highly muscular tunica media.…”

Section: Abnormal Placentation and Placental Ischemiamentioning

confidence: 99%

New Aspects in the Pathophysiology of Preeclampsia

Davison¹,

Homuth²,

Jeyabalan³

et al. 2004

Journal of the American Society of Nephrology

171

109

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Abstract. Preeclampsia, the de novo occurrence of hypertension and proteinuria after the 20th week of gestation, continues to exert an inordinate toll on mothers and children alike. Recent clinical trials, new physiologic insights, and novel observations on pathogenesis have altered the thinking about preeclampsia. The mechanisms surrounding relaxin and its effects on the circulation and on matrix metalloproteinases have been elucidated. The growth factor's receptor, fms-like tyrosine kinase 1, has been shown to exist in a soluble form that is able to inactivate vascular endothelial-derived growth factor and human placental growth factor. Compelling evidence has been brought forth suggesting that fms-like tyrosine kinase 1 is a circulating factor that can cause preeclampsia. Preeclamptic women have high circulating levels of asymmetric dimethyl arginine that could account for the generalized endothelial dysfunction observed in preeclampsia. Preeclamptic women also produce novel autoantibodies that may serve to activate angiotensin receptors. These new observations raise the possibility that the treatment of preeclamptic women will soon be improved.The term preeclampsia refers to the new onset of hypertension (Ͼ140/90 mmHg) and proteinuria after 20 wk of gestation in previously normotensive, nonproteinuric women (1). The condition is common and occurs in~5% of pregnancies in the United States and Europe. Eclampsia is a life-threatening complication and is characterized by grand mal seizures. The term comes from the Greek word for lightning. A severe variant of preeclampsia also features hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). This condition occurs iñ 1 per 1000 pregnancies. Predisposing factors are a positive family history, hypertension, diabetes, preexisting renal disease, multiple pregnancies, and a poor obstetric history. Nephrologists are often called on to see preeclamptic women because of the severe BP elevation and renal disease. Thus, new clinical or experimental information on this condition is important information for nephrologists. Preeclampsia and Subsequent Cardiovascular RiskThe relevance of preeclampsia to the offspring is well recognized. Children who are born to preeclamptic mothers commonly have low birth weight, and their subsequent cardiovascular risk has been a vast investigational field. The mother's outcome has attracted less interest. Chesley, the father of modern preeclampsia research, was of the opinion that once the condition was over, the mothers had no greater risk of adverse long-term outcomes than women without preeclampsia from the general population (2). This issue may prove to be the only matter in which Chesley's opinion was erroneous. Several recent studies suggest that the converse is the case. Smith et al. (3) studied the pregnancy complications and the maternal risk of ischemic cardiac death in 129,290 births. They found that delivering an infant with low birth weight for gestational age increased the hazard ratio for ischemic heart disease o...

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“…25,26 Although the etiology of the disease remains unclear, it is accepted that the placenta has a central role in its pathogenesis, as its removal at delivery results in dissolution of the maternal symptoms. Typical hallmarks of PE include increased trophoblast cell death and a hyperproliferative immature phenotype of the trophoblast cells, 27 which are in part due to a status of oxidative stress. 9,14,28,29 These altered cellular events largely contribute to increased trophoblast turnover, hypothesized to be one of the primary culprits of the generalized maternal endothelial dysfunction responsible for the onset of clinical symptoms.…”

mentioning

confidence: 99%

Mtd/Bok takes a swing: proapoptotic Mtd/Bok regulates trophoblast cell proliferation during human placental development and in preeclampsia

et al. 2009

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We have previously reported that matador/Bcl-2 ovarian killer (Mtd/Bok), a proapoptotic member of the Bcl-2 family, regulates human trophoblast apoptosis and that its levels are elevated in severe preeclamptic pregnancy. Herein, we show that Mtd is also involved in the regulation of proliferation in normal and pathological placentae. Mtd was found in proliferating trophoblast cells during early placental development and in preeclampsia (PE). The main isoform of Mtd associated with trophoblast proliferation was Mtd-L, the full-length isoform, which preferentially localized to the nuclear compartment in proliferating cells, whereas during apoptosis it switched localization to the cytoplasm where it associated with mitochondria. Mtd expression in proliferating cells colocalized with cyclin E1, a G 1 /S phase cell cycle regulator. MtdL-specific knockdown in the early first trimester villous explants and in HEK293 revealed a direct effect of Mtd-L on cyclin E1 expression and cell cycle progression. We conclude that Mtd-L functions to regulate trophoblast cell proliferation during early placentation and that the elevated levels of Mtd found in PE may contribute to increased trophoblast proliferation accompanying this devastating disorder of pregnancy.

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Morphological Changes of the Spiral Arteries in the Placentae Bed in Relation to Pre‐eclampsia and Fetal Growth Retardation

Cited by 347 publications

References 14 publications

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

N-acetylglucosaminyltransferase V inhibits the invasion of trophoblast cells by attenuating MMP2/9 activity in early human pregnancy

New Aspects in the Pathophysiology of Preeclampsia

Mtd/Bok takes a swing: proapoptotic Mtd/Bok regulates trophoblast cell proliferation during human placental development and in preeclampsia

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