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Your search keyword '"Herse, Florian"' showing total 35 results
Start Over Author "Herse, Florian" Publisher elsevier b.v.
35 results on '"Herse, Florian"'

9. 118. Significant increase of soluble B7-H4 in women at high-risk for preeclampsia in the first trimester: A potential immunological biomarker for immunologically-mediated pregnancy complications?

Author

Gellhaus, Alexandra, Mach, Pawel, Nolte-Bönigk, Louisa, Droste, Leonie, Fox, Laura, Frank, Mirjam, Schmidt, Börge, Herse, Florian, Verlohren, Stefan, Wicherek, Lukasz, Iannaccone, Antonella, Birdir, Cahit, Andrikos, Dimitrios, Kimmig, Rainer, and Köninger, Angela

Published
2018
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17. Soluble (pro)renin receptor in preeclampsia and diabetic pregnancies.

Author

Sugulle, Meryam, Heidecke, Harald, Maschke, Ulrike, Herse, Florian, Danser, A.H. Jan, Mueller, Dominik N., Staff, Anne Cathrine, and Dechend, Ralf

Abstract

Women with preexisting or gestational diabetes mellitus have an increased risk for developing preeclampsia. Diabetes and pregnancy are both characterized by very high prorenin levels and renin-angiotensin system activation. Prorenin bound to the (pro)renin receptor has enzymatic activity. We hypothesized that soluble (pro)renin receptor levels are elevated in high-risk pregnancies. Third trimester maternal blood samples from complicated pregnancies (n = 165), (preeclampsia [n = 76], diabetes mellitus [type I diabetes, n = 35; type II diabetes, n = 11; gestational diabetes mellitus, n = 43]), and healthy pregnancies (n = 49) were analyzed for prorenin, renin, and soluble (pro)renin receptor. There were no significant differences in prorenin or renin levels between the study groups in a multivariate model. In the group of women with gestational diabetes, soluble (pro)renin receptor concentrations were significantly higher compared with healthy pregnancies or preeclampsia. Soluble (pro)renin receptor did not correlate with renin or prorenin levels for any of the study groups. Our results show that soluble (pro)renin receptor is dysregulated in pregnancies affected by diabetes mellitus, but not in preeclampsia. Alterations in circulating soluble (pro)renin receptor are unrelated to renin/prorenin in pregnancy, but may be of pathophysiological relevance in diabetic pregnancies in a renin-angiotensin system-independent manner. [ABSTRACT FROM AUTHOR]

Published
2017
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25. Maternal angiotensin increases placental leptin in early gestation via an alternative RAS-pathway - suggesting a link to pre-eclampsia.

Author

Nonn, Olivia, Fischer, Cornelius, Geisberger, Sabrina, El-Heliebi, Amin, Kroneis, Thomas, Forstner, Désirée, Desoye, Gernot, Staff, Anne Cathrine, Sugulle, Meryam, Dechend, Ralf, Pecks, Ulrich, Kollmann, Martina, Stern, Christina, Cartwright, Judith E., Whitley, Guy S., Thilaganathan, Basky, Wadsack, Christian, Huppertz, Berthold, Herse, Florian, and Gauster, Martin

Published
2021
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30. Vitamin D depletion does not affect key aspects of the preeclamptic phenotype in a transgenic rodent model for preeclampsia.

Author

Andersen, Louise Bjørkholt, Golic, Michaela, Przybyl, Lukasz, Sorensen, Grith Lykke, Jørgensen, Jan Stener, Fruekilde, Palle, von Versen-Höynck, Frauke, Herse, Florian, Højskov, Carsten Schriver, Dechend, Ralf, Christesen, Henrik Thybo, and Haase, Nadine

Abstract

Maternal vitamin D deficiency is proposed as a risk factor for preeclampsia in humans. We tested the hypothesis that vitamin D depletion aggravates and high supplementation ameliorates the preeclampsia phenotype in an established transgenic rat model of human renin-angiotensin system–mediated preeclampsia. Adult rat dams, transgenic for human angiotensinogen ( hAGT ) and mated with male rats transgenic for human renin ( hREN ), were fed either vitamin D-depleted chow (VDd) or enriched chow (VDh) 2 weeks before mating and during pregnancy. Mean blood pressure was recorded by tail-cuff, and 24-hour urine samples were collected in metabolic cages at days 6 and 18 of gestation. Rats were sacrificed at day 21 of gestation. Depleted dams (VDd) had negligible serum 25-hydroxyvitamin D 2+3 levels (mean ± SEM; 2.95 ± 0.45 nmol/l vs. VDh 26.20 ± 2.88 nmol/l, P = .01), but in both groups, levels of 1,25(OH) 2 D 3 remained below detection level of 25 pmol/l. Dietary vitamin D depletion did not aggravate hypertension (mean ± SEM BP, day 20 of gestation: 151.38 ± 5.65 mmHg VDd vs. 152.00 ± 4.10 mmHg VDh) or proteinuria. Fetal anthropometrics were similar between the groups, whereas VDd displayed lower placental:fetal weight ratios (0.15 vs. 0.16 g/g, P = .01) and increased sFlt-1/PlGF ratio. Expression of hREN was lower in placenta of VDd dams (0.82 ± 0.44 AU vs. 1.52 ± 0.15 AU, P = .04). Expression of key vitamin D metabolizing enzymes was unchanged. Dietary vitamin D intervention did not alter key aspects of the preeclampsia phenotype using the transgenic rodent model of human renin-angiotensin system–mediated pre-eclampsia, plausibly due to altered vitamin D metabolism or excretion in the transgenic rats. [ABSTRACT FROM AUTHOR]

Published
2016
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34. Platelet-derived factors dysregulate placental sphingosine-1-phosphate receptor 2 in human trophoblasts.

Author

Lyssy, Freya, Guettler, Jacqueline, Brugger, Beatrice A, Stern, Christina, Forstner, Désirée, Nonn, Olivia, Fischer, Cornelius, Herse, Florian, Wernitznig, Stefan, Hirschmugl, Birgit, Wadsack, Christian, and Gauster, Martin

Subjects
*SPHINGOSINE-1-phosphate, *PLACENTA, *POLYMERASE chain reaction, *BLOOD platelet activation, *ENDOTHELIAL cells
Abstract

Sphingosine-1-phosphate (S1P) is an essential and bioactive sphingolipid with various functions, which acts through five different G-protein-coupled receptors (S1PR1–5). What is the localization of S1PR1–S1PR3 in the human placenta and what is the effect of different flow rates, various oxygen concentrations and platelet-derived factors on the expression profile of S1PR in trophoblasts? Expression dynamics of placental S1PR1–S1PR3 were determined in human first trimester (n = 10), pre-term (n = 9) and term (n = 10) cases. Furthermore, the study investigated the expression of these receptors in different primary cell types isolated from human placenta, verified the findings with publicly available single-cell RNA-Seq data from first trimester and immunostaining of human first trimester and term placentas. The study also tested whether the placental S1PR subtypes are dysregulated in differentiated BeWo cells under different flow rates, different oxygen concentrations or in the presence of platelet-derived factors. Quantitative polymerase chain reaction revealed that S1PR2 is the predominant placental S1PR in the first trimester and reduces towards term (P < 0.0001). S1PR1 and S1PR3 increased from first trimester towards term (P < 0.0001). S1PR1 was localized in endothelial cells, whereas S1PR2 and S1PR3 were predominantly found in villous trophoblasts. Furthermore, S1PR2 was found to be significantly down-regulated in BeWo cells when co-incubated with platelet-derived factors (P = 0.0055). This study suggests that the placental S1PR repertoire is differentially expressed across gestation. S1PR2 expression in villous trophoblasts is negatively influenced by platelet-derived factors, which could contribute to down-regulation of placental S1PR2 over time of gestation as platelet presence and activation in the intervillous space increases from the middle of the first trimester onwards. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2023
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