Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Wadsack, Christian  (8)
Type of Medium
Language
Year
  • 1
    In: Clinical Endocrinology, January 2014, Vol.80(1), pp.65-72
    Description: Byline: Mireille N. M. Poppel, Willibald Zeck, Daniela Ulrich, Eva-Christina Schest, Birgit Hirschmugl, Uwe Lang, Christian Wadsack, Gernot Desoye Summary Objective Chemerin is a novel adipokine implicated in inflammation and obesity. We hypothesized that foetal chemerin would be elevated in gestational diabetes mellitus (GDM) and correlate with foetal and maternal adiposity. Design Observational, longitudinal study. Subjects and measurements Foetal chemerin was measured separately in arterial and venous cord blood of 30 infants born to mothers with (n = 15) and without GDM (n = 15), in their mothers in early third trimester and at delivery and in amniotic fluid (week 32) of women with GDM. Expression of chemerin and its receptor in human foetal tissues commercially available and in placental cells was measured by quantitative PCR. Associations between foetal and maternal anthropometric and metabolic variables were assessed in multivariate regression models. Results In GDM, foetal arterial but not venous cord blood chemerin levels were elevated by about 60% (P 0ae05). Venous cord blood chemerin was higher in infants of obese women (P 0ae01). In multivariate analyses, neither amniotic fluid nor cord blood chemerin levels correlated with birth weight or ponderal index. Both arterial and venous chemerin levels were related to maternal chemerin at birth, and arterial chemerin was associated with GDM status in addition. Maternal levels were unaltered in GDM, but higher in maternal obesity. Foetal liver produces fourfold more chemerin mRNA than other foetal tissues, whereas its receptor prevails in spleen. Conclusions Based on multivariate analyses, foetal growth appears unrelated to foetal chemerin. Maternal obesity and GDM have differential effects on foetal chemerin levels. Site of major production (liver) and action (spleen) differ in human foetal tissues. Article Note: Equal contribution of both authors.
    Keywords: Obesity -- Analysis ; Gestational Diabetes -- Analysis ; Rna -- Analysis;
    ISSN: 0300-0664
    E-ISSN: 1365-2265
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: Placenta, September 2017, Vol.57, pp.293-293
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.placenta.2017.07.220 Byline: Birgit Hirschmugl, Michael Gruber, Uwe Lang, Gernot Desoye, Christian Wadsack Author Affiliation: Medical University of Graz, Department of Obstetrics and Gynecology, Graz, Austria Article Note: (miscellaneous) P2.02
    Keywords: Medicine ; Anatomy & Physiology ; Zoology
    ISSN: 0143-4004
    E-ISSN: 1532-3102
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: Physiological genomics, 21 November 2011, Vol.43(22), pp.1255-62
    Description: Maternal lipoproteins have been studied extensively in human pregnancies, but little is known about the role of fetal lipoproteins. The vascularized human placenta interfaces between the mother and fetus to transfer nutrients for sustaining pregnancy. Unlike that of adults, fetal high-density lipoprotein (HDL), which is in contact with placental vessels, is characterized by a high proportion of apolipoprotein E (apoE). We hypothesize this unique composition of fetal HDL affects key functions of the growing fetal tissues. The aim was to identify genes regulated by apoE-HDL by incubating human placental endothelial cells (HPEC) with either fetal HDL or apoE-rich reconstituted HDL particles (apoE-rHDL). HPEC were exposed to 15 μg/ml fetal HDL, 15 μg/ml apoE-rHDL, or medium for 16 h, respectively. Microarray analysis determined genes regulated by fetal HDL and apoE. Characterization of HDL particles revealed a different hydrodynamic radius for apoE-rHDL (13.70 nm) compared with fetal HDL (18.11 nm). Stepwise gene clustering after microarray experiments identified 79 differentially expressed genes (P 〈 0.05) when cells were exposed to HDL compared with controls. Among them 16 genes were downregulated, whereas five genes were upregulated by twofold, respectively. When HPEC were incubated with apoE-rHDL 18-fold more genes (1,417, 12% of transcripts) were regulated (P 〈 0.05) in contrast to HDL. Thereof, 172 genes were downregulated and 376 genes upregulated (twofold). In the common subset of 38 genes regulated by both HDL particles, genes involved in cholesterol biosynthesis and cell protection prevailed. Strikingly, results suggest that HDL has the capability of regulating metallothioneins, which may have an effect on oxidative stress in HPEC.
    Keywords: Gene Expression Regulation ; Apolipoproteins E -- Genetics ; Endothelial Cells -- Metabolism ; Lipoproteins, HDL -- Genetics ; Placenta -- Metabolism
    ISSN: 10948341
    E-ISSN: 1531-2267
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Language: English
    In: Sci Rep, 2017, Vol.7(1), pp.12628-12628
    Description: Increased Lipoprotein associated phospholipase A (LpPLA) has been associated with inflammatory pathologies, including Type 2 Diabetes. Studies on LpPLA and Gestational Diabetes Mellitus (GDM) are rare, and have focused mostly on maternal outcome. In the present study, we investigated whether LpPLA activity on foetal lipoproteins is altered by maternal GDM and/or obesity (a major risk factor for GDM), thereby contributing to changes in lipoprotein functionality. We identified HDL as the major carrier of LpPLA activity in the foetus, which is in contrast to adults. We observed marked expression of LpPLA in placental macrophages (Hofbauer cells; HBCs) and found that LpPLA activity in these cells was increased by insulin, leptin, and pro-inflammatory cytokines. These regulators were also increased in plasma of children born from GDM pregnancies. Our results suggest that insulin, leptin, and pro-inflammatory cytokines are positive regulators of LpPLA activity in the foeto-placental unit. Of particular interest, functional assays using a specific LpPLA inhibitor suggest that high-density lipoprotein (HDL)-associated LpPLA exerts anti-oxidative, athero-protective functions on placental endothelium and foetus. Our results therefore raise the possibility that foetal HDL-associated LpPLA might act as an anti-inflammatory enzyme improving vascular barrier function.
    Keywords: Biology;
    ISSN: 2045-2322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: Placenta, September 2016, Vol.45, pp.103-103
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.placenta.2016.06.148 Byline: Pablo Zardoya-Laguardia, Astrid Blaschitz, Birgit Hirschmugl, Ingrid Lang, Martin Gauster, Martin Hausler, Mila Cervar-Zivkovic, Eva Karpf, Christian Wadsack, Sasa Frank, Peter Sedlmayr Author Affiliation: (1) Institute of Cell Biology, Histology and Embryology, Graz, Styria, Austria (2) Department of Obstetrics and Gynaecology, Graz, Styria, Austria (3) Institute of Pathology, Graz, Styria, Austria (4) Institute of Molecular Biology and Biochemistry, Graz, Styria, Austria Article Note: (miscellaneous) P1.103
    Keywords: Medicine ; Anatomy & Physiology ; Zoology
    ISSN: 0143-4004
    E-ISSN: 1532-3102
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Language: English
    In: Placenta, September 2017, Vol.57, pp.270-270
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.placenta.2017.07.154 Byline: Pablo Zardoya-Laguardia (1), Astrid Blaschitz (1), Birgit Hirschmugl (2), Ingrid Lang (1), Sereina Herzog (3), Liudmila Nikitina (1), Martin Gauster (1), Martin Hausler (2), Mila Cervar-Zivkovic (1), Eva Karpf (4), Ghassan Maghzal (5)(6), Chris Stanley (5), Roland Stocker (5)(6), Christian Wadsack (2), Sasa Frank (7), Peter Sedlmayr (1) Author Affiliation: (1) Medical University of Graz, Institute of Cell Biology, Histology and Embryology, Graz, Styria, Austria (2) Medical University of Graz, Department of Obstetrics and Gynaecology, Graz, Styria, Austria (3) Medical University of Graz, Institute for Medical Informatics, Statistics and Documentation, Graz, Styria, Austria (4) Medical University of Graz, Institute of Pathology, Graz, Styria, Austria (5) Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia (6) University of New South Wales, School of Medical Sciences, Sydney, New South Wales, Australia (7) Medical University of Graz, Institute of Molecular Biology and Biochemistry, Graz, Styria, Austria Article Note: (miscellaneous) P1.66
    Keywords: Medicine ; Anatomy & Physiology ; Zoology
    ISSN: 0143-4004
    E-ISSN: 1532-3102
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Scientific reports, 03 April 2018, Vol.8(1), pp.5488
    Description: Indoleamine 2,3-dioxygenase-1 (IDO1) mediates the degradation of L-tryptophan (L-Trp) and is constitutively expressed in the chorionic vascular endothelium of the human placenta with highest levels in the microvasculature. Given that endothelial expression of IDO1 has been shown to regulate vascular tone and blood pressure in mice under the condition of systemic inflammation, we asked whether IDO1 is also involved in the regulation of placental blood flow and if yes, whether this function is potentially impaired in intrauterine growth restriction (IUGR) and pre-eclampsia (PE). In the large arteries of the chorionic plate L-Trp induced relaxation only after upregulation of IDO1 using interferon gamma and tumor necrosis factor alpha. However, ex vivo placental perfusion of pre-constricted cotyledonic vasculature with L-Trp decreases the vessel back pressure without prior IDO1 induction. Further to this finding, IDO1 protein expression and activity is reduced in IUGR and PE when compared to gestational age-matched control tissue. These data suggest that L-Trp catabolism plays a role in the regulation of placental vascular tone, a finding which is potentially linked to placental and fetal growth. In this context our data suggest that IDO1 deficiency is related to the pathogenesis of IUGR and PE.
    Keywords: Blood Vessels -- Physiopathology ; Endothelium, Vascular -- Enzymology ; Fetal Growth Retardation -- Enzymology ; Placenta -- Blood Supply ; Pre-Eclampsia -- Enzymology
    E-ISSN: 2045-2322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    In: Circulation Research, 2009, Vol.104(5), pp.600-608
    Description: Although maternal–fetal cholesterol transfer may serve to compensate for insufficient fetal cholesterol biosynthesis under pathological conditions, it may have detrimental consequences under conditions of maternal hypercholesterolemia leading to preatherosclerotic lesion development in fetal aortas. Maternal cholesterol may enter fetal circulation by traversing syncytiotrophoblast and endothelial layers of the placenta. We hypothesized that endothelial cells (ECs) of the fetoplacental vasculature display a high and tightly regulated capacity for cholesterol release. Using ECs isolated from human term placenta (HPECs), we investigated cholesterol release capacity and examined transporters involved in cholesterol efflux pathways controlled by liver-X-receptors (LXRs). HPECs demonstrated 2.5-fold higher cholesterol release to lipid-free apolipoprotein (apo)A-I than human umbilical vein ECs (HUVECs), whereas both cell types showed similar cholesterol efflux to high-density lipoproteins (HDLs). Interestingly, treatment of HPECs with LXR activators increased cholesterol efflux to both types of acceptors, whereas no such response could be observed for HUVECs. In line with enhanced cholesterol efflux, LXR activation in HPECs increased expression of ATP-binding cassette transporters ABCA1 and ABCG1, while not altering expression of ABCG4 and scavenger receptor class B type I (SR-BI). Inhibition of ABCA1 or silencing of ABCG1 decreased cholesterol efflux to apoA-I (−70%) and HDL3 (−57%), respectively. Immunohistochemistry localized both transporters predominantly to the apical membranes of placental ECs in situ. Thus, ECs of human term placenta exhibit unique, efficient and LXR-regulated cholesterol efflux mechanisms. We propose a sequential pathway mediated by ABCA1 and ABCG1, respectively, by which HPECs participate in forming mature HDL in the fetal blood.
    Keywords: Maternal-Fetal Exchange ; ATP-Binding Cassette Transporters -- Metabolism ; Cholesterol -- Metabolism ; Endothelial Cells -- Metabolism ; Placenta -- Blood Supply;
    ISSN: 0009-7330
    E-ISSN: 15244571
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages