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001-es BibID:	BIBFORM065224
Első szerző:	Lázár Levente (szülész-nőgyógyász)
Cím:	Role of hsa-miR-325 in the etiopathology of preeclampsia / Levente Lázár, Bálint Nagy, Attila Molvarec, András Szarka, János Rigó
Dátum:	2012
ISSN:	1791-2997 1791-3004
Megjegyzések:	Preeclampsia (PE) is a common pregnancy-specific syndrome characterized by hypertension and proteinuria. Evidence has demonstrated that hypertensive disorders in pregnancy are associated with alterations in the expression of different microRNAs (miRNAs). miRNAs are endogenously expressed non-coding RNAs that have significant biological and pathological functions due to their potential mechanisms of regulation of gene expression. The purpose of the present study was to investigate the expression of hsa-miR-325 in placental samples of preeclamptic and uncomplicated pregnancy patients. hsa-miR-325 was isolated from placenta tissue samples obtained from 31 preeclamptic and 28 normotensive pregnant females. Quantitative real-time polymerase chain reaction was used to analyze miRNA expression. The expression of hsa-miR?325 was elevated in uncomplicated pregnancies compared with preeclamptic patients. ?Ct (mean ? SD) values were 0.117?0.07 in PE tissues and 0.135?0.051 in normotensive cases (p<0.05). The expression levels correlated with patient blood pressure (p=0.015, r=-0.23), and tended to correlate with body mass index (p=0.065, r=0.261). The expression of hsa-miR-325 was downregulated in the case of PE. Changes in hsa-miR?325 expression in the case of pregnancy-related hypertensive disorders might affect the oxidative stress pathways and heat-shock protein production. These factors have a strong correlation with the development of PE. We, therefore, suggest that hsa-miR-325 contributes to the pathogenesis of PE.IntroductionHypertensive disorders are a leading cause of perinatal morbidity and mortality in pregnancy. Preeclampsia (PE) is a common pregnancy-specific syndrome that affects at least 5% of all pregnancies worldwide (1,2). It is characterized by hypertension (RR ?140/90 mmHg) and proteinuria of ?300 mg/24 h, developing after midgestation in previously normotensive pregnant females. Although the exact etiology of PE remains unknown, pathological studies have demonstrated the abnormal development of an ischemic placenta (2). Shallow endovascular trophoblast invasion in the spiral arteries and generalized endothelial cell dysfunction are key factors, while placental ischemia, oxidative stress and maternal-fetal immune maladaptation affect the development of PE. The only treatment is delivery of the placenta, after which the symptoms regress rapidly. Evidence has demonstrated that hypertensive disorders in non-pregnant and pregnant patients are associated with alterations in different miRNA expressions of specific tissues (3?5).miRNAs are non-protein coding RNAs, and functionally negative regulators of gene expression by antisense complementarity to specific messenger RNAs (6,7). They act by targeting the RNA-induced silencing complex to complementary sites within the 3·-untranslated region (UTR) of their target mRNAs. Depending on the degree of base pairing between the miRNA and the 3·-UTR, either degradation or translational repression of the targeted mRNA occurs. Although they account for less than 1% of all human genes, miRNAs have been estimated to regulate up to 30% of all protein-encoding genes (8). Their best-known representatives are the 18?24 nucleotide long single-stranded miRNA. The mean number of copies per cell is between 10 and 50000, depending on the tissue and the miRNA (9,10).Few studies have presented data regarding a comprehensive list of the human miRNAs expressed in the placenta and the possible roles of the different miRNAs in the pathophysiology of pregnancy-related disorders (11?13). Taking into consideration the high number of miRNAs, further studies regarding the expression of different miRNA in pregnancy-related hypertensive disorders may be important in understanding the pathophysiology of this disease.In the present study, we performed a real-time polymerase chain reaction PCR analysis of hsa-miR-325. hsa-miR-325 is located at Xq21.1. Different databases (http://www.mirdb.org; http://www.nextprot.org) were evaluated, and hsa-miR-325 was selected as it is a non-studied miRNA that targets genes and candidate protein regulatory pathways affecting different etiological factors, including body mass index (BMI), blood pressure regulation, oxidative stress, endometrial function and heat-shock protein regulation, thus playing a key role in the development of hypertensive disorders in pregnancy.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban miRNA Preeclampsia gene expression
Megjelenés:	Molecular Medicine Reports 6 (2012), p. 597-600. -
További szerzők:	Nagy Bálint (1956-) (molekuláris genetikus) Molvarec Attila (szülész-nőgyógyász) Szarka András Rigó János (1958-) (szülész-nőgyógyász)
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001-es BibID:	BIBFORM065232
Első szerző:	Molvarec Attila (szülész-nőgyógyász)
Cím:	Circulating angiogenic factors determined by electrochemiluminescence immunoassay in relation to the clinical features and laboratory parameters in women with pre-eclampsia / Attila Molvarec, András Szarka, Szilvia Walentin, Endre Szűcs, Bálint Nagy, János Rigó Jr.
Dátum:	2010
ISSN:	0916-9636
Megjegyzések:	The purpose of this study was to determine whether increased serum soluble fms-like tyrosine kinase-1 (sFlt-1) and decreasedplacental growth factor (PlGF) levels in pre-eclampsia are related to the clinical features and laboratory parameters of thepatients, including markers of inflammation, endothelial activation and injury, oxidative stress and trophoblast debris. A total of54 pre-eclamptic patients, 58 healthy pregnant and 52 healthy non-pregnant women were involved in this case?control study.Serum sFlt-1 and PlGF levels were measured by electrochemiluminescence immunoassay. Serum levels of sFlt-1 and PlGF weresignificantly higher in pre-eclamptic patients and healthy pregnant women than in healthy non-pregnant women. In addition,pre-eclamptic patients had significantly higher sFlt-1 levels and significantly lower PlGF concentrations compared with healthy pregnant women. According to the subgroup analyses, sFlt-1 levels were significantly higher in severely pre-eclamptic patients than in those with mild pre-eclampsia, whereas pre-eclamptic patients with fetal growth restriction or preterm onset of the disease had significantly lower PlGF concentrations compared with those without intrauterine growth restriction or with a diseaseonset at term. In the pre-eclamptic group, there were significant positive correlations between serum sFlt-1 levels and systolic and diastolic blood pressure, serum levels of blood urea nitrogen and creatinine, as well as plasma levels of von Willebrand factor antigen, fibronectin and cell-free fetal DNA. Furthermore, serum PlGF concentrations of pre-eclamptic patients showedsignificant positive correlations with gestational age at disease onset and delivery, as well as with fetal birth weight, and significant inverse correlations with levels of blood urea nitrogen, creatinine and fibronectin. In conclusion, increased serum sFlt-1 and decreased PlGF levels are associated with blood pressure, renal and endothelial dysfunction, trophoblast deportation, as well as with a shorter duration of pregnancy, fetal growth restriction, the severity and preterm onset of the disease in pre-eclampsia. These findings indicate the central role of an angiogenic imbalance in the pathogenesis of this pregnancy-specific disorde
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban circulating Angiogenic preeclampsia factors
Megjelenés:	Hypertension Research 33 : 9 (2010), p. 892-898. -
További szerzők:	Szarka András Walentin Szilvia Szűcs Endre Nagy Bálint (1956-) (molekuláris genetikus) Rigó János (1958-) (szülész-nőgyógyász)
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