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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Reversal of the normal diurnal blood pressure pattern has been demonstrated in women with severe hypertension and renal impairment in pregnancy (pre-eclampsia). 2. Maximum arterial pressure occurred at night in these women. The phenomenon was not due to hypotensive drug therapy or posture. Patients with uncomplicated essential hypertension in pregnancy retained a normal diurnal blood pressure pattern. 3. Nocturnal hypertension in pre-eclampsia is of theoretical interest and practical importance.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Reversed diurnal blood pressure rhythm in hypertensive pregnancies. 107 9

The proliferation of villous trophoblast in the human placenta was estimated throughout normal gestation and in term placentae from preeclamptic and smoking mothers by two different methods. These were: 1) labeling of DNA producing cells by bromodeoxyuridine (BrdU) followed by immunohistochemistry using a monoclonal anti-BrdU antibody, and 2) immunohistochemical identification of all proliferating cells by the monoclonal antibody Ki67. Both methods revealed comparable results. In uncomplicated pregnancies there was a remarkable decrease in the labeling indices from early gestation to term. This was the result of a diminution of the number of Langhans' cells, although the cell division rate within the Langhans' cell layer remained nearly constant throughout gestation. A prolongation of the cell cycle in the cytotrophoblast cells at term was indicated by an increase in the Ki67/BrdU ratio. Compared with normal term placentae, there was an increase in the trophoblast proliferation rate in preeclampsia, but not in placentae from smoking mothers. Moreover, the number of Langhans' cells was diminished in placentae from smokers. The results indicate that there are different pathogenetic mechanisms of placental impairment in preeclampsia and in maternal smoking. In preeclampsia an injury to the syncytiotrophoblast seems to lead to a repair hyperplasia of the cytotrophoblast, whereas in maternal smoking, there seems to be a direct toxic effect on the cytotrophoblastic cells.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Proliferation of villous trophoblast of the human placenta in normal and abnormal pregnancies. 168 53

The aim of the study was to compare the binding of endothelin-1 (ET-1) to membranes from placental tissue and trophoblast cells in normal and pre-eclamptic pregnancies. Plasma membranes from placental tissue and trophoblastic cells were prepared from 15 control and 18 pre-eclamptic pregnancies at either preterm (weeks 31-36) or term (weeks 37-40). ET-1 binding to tissue membranes was measured by a radioreceptor assay. In addition, binding of 56 nmol/l [125I]ET-1 to plasma membranes of trophoblastic cells was determined. In pre-eclampsia, placental membranes bound less (P < 0.01) ET-1 owing to fewer (P < 0.01) receptors at preterm than in the corresponding preterm controls. In contrast, binding of [125I]ET-1 to plasma membranes of trophoblast cells was higher (P < 0.01) in pre-eclampsia at both gestational stages than in the controls. Incubation of trophoblast cells with hydralazine reduced binding by 70%. We conclude that pre-eclampsia is associated with changes in the binding of ET-1 to its placental receptors. Moreover, the data suggest that pre-eclampsia affects non-trophoblast cells in the opposite manner to the trophoblast.
Mol Cell Endocrinol 1995 Apr 28
PMID:Pre-eclampsia and gestational age differently alter binding of endothelin-1 to placental and trophoblast membrane preparations. 767 54

Pregnancy-induced hypertension (PIH) is a frequent cause of maternal and neonatal morbidity and mortality. In the present study we focused on the pathophysiology of PIH, mainly on the role of mineralocorticoids, reversed blood pressure patterns, and the resulting necessity of continuous monitoring of the preeclamptic mother. Problems of antihypertensive therapy are discussed and the first results of a pilot study with Urapidil are presented. To examine the role of mineralocorticoids in the pathophysiology of PIH, we studied plasma aldosterone and 18-hydroxy-corticosterone (18-OH-B) levels in 25 women with PIH and in 25 healthy pregnant women. Furthermore, we evaluated the mineralocorticoid receptor (MR) count in mononuclear leukocytes in the 2 groups. The MR-count was significantly decreased in the PIH-group. The values of plasma aldosterone and 18-OH-B were also low. These results cannot be explained by receptor down-regulation due to higher level of mineralocorticoids of the zona glomerulosa. Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered MR-status. The first results of continuous blood pressure measurements with a noninvasive, real-time blood pressure monitor (Finapres) are presented. The comparison of the obtained values with intraarterial measurements demonstrates a good correlation between the two methods. We also report on the first experiences with Urapidil in the treatment of hypertension in severe preeclampsia. The data show that hypertension in preeclamptic women can be treated by Urapidil without side effects or reflex-tachycardia. Further studies will have to prove if Urapidil is suited for prepartal treatment of PIH as well.
J Steroid Biochem Mol Biol 1993 Apr
PMID:Hypertension in pregnancy. 838 33

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) > or = 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).
Mol Cell Biochem 1995 Oct 04
PMID:Relationship between elevated lipid peroxides, vitamin E deficiency and hypertension in preeclampsia. 858 11

Lipid peroxides and their related free radicals have been implicated in the pathogenesis of placental dysfunction in preeclampsia. Recent studies suggest that the placenta is a source of the increased lipid peroxides in the maternal circulation of women with preeclampsia. We examined intracellular localization of 4-hydroxy-2-nonenal (HNE: a major aldehydic product of lipid peroxidation)-modified proteins in human placentas by immunohistochemistry, and immunoblotting. The trophoblast layer of the chorionic villi showed intense immunoreactivity for HNE-modified proteins in 4 of 12 preeclamptic placentas, whereas no staining was observed in 12 normal placentas. Immunoblotting revealed that three immunoreactive proteins with apparent molecular mass of 110 kDa, 75 kDa, and 70 kDa were localized in the mitochondrial fraction. The present results indicate that the damage to mitochondrial proteins by lipid peroxidation by products and subsequent dysfunction of trophoblasts contribute to the pathophysiology of preeclampsia.
Biochem Mol Biol Int 1997 Apr
PMID:Increased mitochondrial damage by lipid peroxidation in trophoblast cells of preeclamptic placentas. 911 37

In the early 1950s, Medawar proposed the concept of "the fetus as an allograft". Since then, the immunological relationship between the mammalian fetus and its mother during pregnancy has been considered to be similar to that between a transplanted allograft and its recipient. Because of this analogy, it has been assumed that implantation of the fetal placenta in the uterus would similarly be controlled by a maternal immune response mediated by T cells recognizing paternally derived alloantigens expressed by the placenta. Surprisingly, recent evidence suggests that implantation might predominantly involve a novel allogeneic recognition system based on natural killer cells rather than T cells. The cellular and molecular basis of this local immune interaction between the fetal placenta and maternal uterus is now the focus of intense research interest. Because aberrant implantation can cause a variety of clinical problems including miscarriage, intrauterine growth retardation and pre-eclampsia, an understanding of the immunological mechanism by which this process is controlled could lead to the development of regimes to treat these important obstetric conditions.
Mol Med Today 1997 Apr
PMID:Immunology of human placental implantation: clinical implications of our current understanding. 913 28

To obtain some insight into the extracellular matrix in the human placenta, we investigated the composition of collagens purified from the placentae of patients with pre-eclampsia and compared it with normal placentae. Collagen was extracted from the placentae of both normal and pre-eclampsia pregnancies during the third trimester. The relative amounts of various collagens were evaluated by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. The ratio of the intensity of the band corresponding to the alpha 1 (III) chain with that of the alpha 1 (I) chain in placentae of pre-eclampsia was significantly lower than in normal placentae (P < 0.05). In contrast, the ratio of the intensity of the band corresponding to the alpha 1 (V) chain with that of the alpha 1 (I) chain in placentae of pre-eclampsia was significantly higher than in normal placentae (P < 0.05). The results suggest that an increased level of type V collagen relative to type I collagen in the placentae of pre-eclampsia might be closely associated with the disturbance to trophoblastic cell functions and the supply of nutrients to the developing fetus necessary for the maintenance of pregnancy.
Mol Hum Reprod 1997 Aug
PMID:Increase in the relative level of type V collagen in the placentae of patients with pre-eclampsia. 929 58

Toxicosis syndrome of fasting pregnant ewes has a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological factor might be oxidative hemolysis and heme-induced endothelial damage. Ewes (5 starving, 5 control) at 130-135 gestational days with a 96-h fasting period followed by refeeding were used. Blood pressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glucose, hemoglobin/heme, free thiol groups and Trolox equivalent antioxidant capacity, and plasma iron and ferritin levels were measured. Statistical significance was assessed using Student's t test (P < 0.05). Besides hypertension and renal disturbances, hemolysis, elevated liver enzymes and low platelet count, characteristic of human HELLP syndrome, were also present. In the first 24 h of glucose deprivation there was a significant rise in both the plasma hemoglobin/heme and indirect bilirubin concentrations. The antioxidant free thiol levels decreased significantly the next day, without any change in the total antioxidant capacity of the plasma. While the loss of calcium and magnesium levels related to the similarity to preeclampsia, reduced plasma iron concentrations referred to species differences in iron homeostasis. An oxidative stress causing hemolysis in a glucose-6-phosphate dehydrogenase-deficient animal model was proven by the loss of free thiols after glucose deprivation. The activation of the oxidative stress protein heme oxygenase was a signal of endothelial cell injury, the primary cause of pregnancy-induced hypertension.
Biochem Mol Med 1997 Oct
PMID:The pathogenetic role of heme in pregnancy-induced hypertension-like disease in ewes. 936 99

Pre-eclampsia is a common, pregnancy-induced, multisystem disease leading to severe complications in the mother and foetus. The aetiology of pre-eclampsia remains a mystery, but a growing body of evidence suggests that a mitochondrial defect might cause the impairement of differentiation and invasion of the trophoblast that leads to this disorder. This hypothesis is the topic of ongoing studies that, if confirmed, would be highly relevant to preventative strategies for this disease.
Mol Med Today 1998 Jul
PMID:Pre-eclampsia: a disorder of placental mitochondria? 974 89


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