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  • 1
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    Bcl10 Mediates Angiotensin II–Induced Cardiac Damage and Electrical Remodeling
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. 5 ( 2014-11), p. 1032-1039
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. 5 ( 2014-11), p. 1032-1039
    Abstract: Angiotensin (Ang) II is a potent mediator of both hypertension and cardiac damage; however, the mechanisms by which this occur remain unclear. B-cell lymphoma/leukemia 10 (Bcl10) is a member of the CBM signalosome, which links Ang II and nuclear factor-κB signaling. We hypothesized that Bcl10 is pivotal in the pathogenesis of Ang II–induced cardiac damage. Ang II infusion in mice lacking Bcl10 resulted in reduced cardiac fibrosis, less cellular infiltration, and improved arrhythmogenic electric remodeling, despite a similar degree of hypertension or cardiac hypertrophy. Adoptive transfer of bone marrow (BM), whereby Bcl10 knockout or wildtype BM was transferred to their opposite genotype recipients, revealed the dual importance of Bcl10 within both cardiac and immune cells. Loss of Bcl10 in cardiac cells resulted in reduced expression of genes important for the adhesion and recruitment of immune cells. In vitro experiments demonstrated that adhesion of monocytes to Ang II–treated endothelial cells also required Bcl10. Additionally, Bcl10 deficiency in macrophages reduced their intrinsic migratory ability. To address the role of BM-derived fibroblasts in the formation of cardiac fibrosis, we explored whether Bcl10 is also important for the infiltration of BM-derived (myo)fibroblasts into the heart. The transfer of green fluorescent protein positive wildtype BM into Bcl10 knockout recipient mice revealed a reduced number of noncardiac (myo)fibroblasts compared with those wildtype recipients. Our results demonstrate the significant role of Bcl10 in multiple cell types important for the generation of Ang II–induced cardiac damage and electric remodeling and may provide a new avenue for therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.114.03900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2094210-2
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  • 2
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    Abstract 560: Vitamin D Depletion Aggravates Hypertension in Transgenic Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. suppl_1 ( 2013-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. suppl_1 ( 2013-09)
    Abstract: Introduction: Vitamin D may ameliorate hypertension and kidney disease through genomic and extra-genomic pathways. Several studies have shown that vitamin D levels can affect levels of circulating FoxP3-positive regulatory T-lymphocytes. Previously, our group has demonstrated that adoptive transfer of FoxP3-positive T-lymphocytes ameliorated the phenotype in a mouse model of angiotensin-II induced cardiac damage. Objective: To investigate the impact of vitamin D depletion in a transgenic rat model of angiotensin II-mediated hypertensive organ failure, and to investigate the possible association with levels of FoxP3 regulatory T-lymphocytes. Methods: In 4-week old age-matched rats overexpressing the human renin and angiotensinogen genes, group 1 (n=18) received vitamin D depleted chow, and group 2, (n=15) received chow with standard contents of vitamin D. Blood pressure (tail cuff) and 24-hour albuminuria were determined once weekly. After three weeks, animals were sacrificed. Heart tissue was examined for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) by RT-PCR. Lymphocytes from spleens were isolated, and the percentage of CD4+ cells, which were CD4+CD25+FoxP3-positive, was measured by flow cytometry. Mesenteric arteries were removed and stimulated with nitroprusside and acetylcholine to investigate the relaxation potential of the epithelium. Results: The vitamin D depleted group had higher blood pressure at all times (mean differences were 23.40 mmHg, 14.31 mmHg and 15.71 mmHg respectively, p 〈 0.05), higher heart-to-body weight ratio, and higher ANP and BNP levels. No differences were found between groups in mortality or proteinuria. Neither the levels of CD4+CD25+FoxP3-positive cells in spleen, nor the relaxation potential measured in mesenteric arteries differed between groups. Conclusion: Short-term vitamin D depletion aggravated hypertension and end-organ damage in a rat model of angiotensin II-induced hypertension. However, the aggravated phenotype was not due to different levels of splenic FoxP3-positive activated T-lymphocytes or to higher endothelial resistance in arteries.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.62.suppl_1.A560
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 3
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    CD74-Downregulation of Placental Macrophage-Trophoblastic Interactions in Preeclampsia
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 119, No. 1 ( 2016-06-24), p. 55-68
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 1 ( 2016-06-24), p. 55-68
    Abstract: We hypothesized that cluster of differentiation 74 (CD74) downregulation on placental macrophages, leading to altered macrophage-trophoblast interaction, is involved in preeclampsia. Objective: Preeclamptic pregnancies feature hypertension, proteinuria, and placental anomalies. Feto-placental macrophages regulate villous trophoblast differentiation during placental development. Disturbance of this well-balanced regulation can lead to pathological pregnancies. Methods and Results: We performed whole-genome expression analysis of placental tissue. CD74 was one of the most downregulated genes in placentas from preeclamptic women. By reverse transcriptase-polymerase chain reaction, we confirmed this finding in early-onset ( 〈 34 gestational week, n=26) and late-onset (≥34 gestational week, n=24) samples from preeclamptic women, compared with healthy pregnant controls (n=28). CD74 protein levels were analyzed by Western blot and flow cytometry. We identified placental macrophages to express CD74 by immunofluorescence, flow cytometry, and RT-PCR. CD74-positive macrophages were significantly reduced in preeclamptic placentas compared with controls. CD74-silenced macrophages showed that the adhesion molecules ALCAM , ICAM4 , and Syndecan-2, as well as macrophage adhesion to trophoblasts were diminished. Naive and activated macrophages lacking CD74 showed a shift toward a proinflammatory signature with an increased secretion of tumor necrosis factor-α, chemokine (C–C motif) ligand 5, and monocyte chemotactic protein-1, when cocultured with trophoblasts compared with control macrophages. Trophoblasts stimulated by these factors express more CYP2J2 , sFlt1 , TNFα , and IL-8 . CD74-knockout mice showed disturbed placental morphology, reduced junctional zone, smaller placentas, and impaired spiral artery remodeling with fetal growth restriction. Conclusions: CD74 downregulation in placental macrophages is present in preeclampsia. CD74 downregulation leads to altered macrophage activation toward a proinflammatory signature and a disturbed crosstalk with trophoblasts.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.116.308304
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Regulatory T Cells Ameliorate Intrauterine Growth Retardation in a Transgenic Rat Model for Preeclampsia
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 65, No. 6 ( 2015-06), p. 1298-1306
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 65, No. 6 ( 2015-06), p. 1298-1306
    Abstract: Preeclampsia is a multisystemic syndrome during pregnancy that is often associated with intrauterine growth retardation. Immunologic dysregulation, involving T cells, is implicated in the pathogenesis. The aim of this study was to evaluate the effect of upregulating regulatory T cells in an established transgenic rat model for preeclampsia. Application of superagonistic monoclonal antibody for CD28 has been shown to effectively upregulate regulatory T cells. In the first protocol (treatment protocol), we applied 1 mg of CD28 superagonist or control antibody on days 11 and 15 of pregnancy. In the second protocol (prevention protocol), the superagonist or control antibody was applied on days 1, 5, and 9. Superagonist increased regulatory T cells in circulation and placenta from 8.49±2.09% of CD4-positive T cells to 23.50±3.05% and from 3.85±1.45% to 23.27±7.64%, respectively. Blood pressure and albuminuria (30.6±15.1 versus 14.6±5.5 mg/d) were similar in the superagonist or control antibody–treated preeclamptic group for both protocols. Rats treated with CD28 superagonist showed increased pup weights in the prevention protocol (2.66±0.03 versus 2.37±0.05 g) and in the treatment protocol (3.04±0.04 versus 2.54±0.1 g). Intrauterine growth retardation, calculated by brain:liver weight ratio, was also decreased by the superagonist in both protocols. Further analysis of brain development revealed a 20% increase in brain volume by the superagonist. Induction of regulatory T cells in the circulation and the uteroplacental unit in an established preeclamptic rat model had no influence on maternal hypertension and proteinuria. However, it substantially improved fetal outcome by ameliorating intrauterine growth retardation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.114.04892
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 5
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    Disturbed Placental Imprinting in Preeclampsia Leads to Altered Expression of DLX5, a Human-Specific Early Trophoblast Marker
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation Vol. 136, No. 19 ( 2017-11-07), p. 1824-1839
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 136, No. 19 ( 2017-11-07), p. 1824-1839
    Abstract: Preeclampsia is a complex and common human-specific pregnancy syndrome associated with placental pathology. The human specificity provides both intellectual and methodological challenges, lacking a robust model system. Given the role of imprinted genes in human placentation and the vulnerability of imprinted genes to loss of imprinting changes, there has been extensive speculation, but no robust evidence, that imprinted genes are involved in preeclampsia. Our study aims to investigate whether disturbed imprinting contributes to preeclampsia. Methods: We first aimed to confirm that preeclampsia is a disease of the placenta by generating and analyzing genome-wide molecular data on well-characterized patient material. We performed high-throughput transcriptome analyses of multiple placenta samples from healthy controls and patients with preeclampsia. Next, we identified differentially expressed genes in preeclamptic placentas and intersected them with the list of human imprinted genes. We used bioinformatics/statistical analyses to confirm association between imprinting and preeclampsia and to predict biological processes affected in preeclampsia. Validation included epigenetic and cellular assays. In terms of human specificity, we established an in vitro invasion-differentiation trophoblast model. Our comparative phylogenetic analysis involved single-cell transcriptome data of human, macaque, and mouse preimplantation embryogenesis. Results: We found disturbed placental imprinting in preeclampsia and revealed potential candidates, including GATA3 and DLX5 , with poorly explored imprinted status and no prior association with preeclampsia. As a result of loss of imprinting, DLX5 was upregulated in 69% of preeclamptic placentas. Levels of DLX5 correlated with classic preeclampsia markers. DLX5 is expressed in human but not in murine trophoblast. The DLX5 high phenotype resulted in reduced proliferation, increased metabolism, and endoplasmic reticulum stress-response activation in trophoblasts in vitro. The transcriptional profile of such cells mimics the transcriptome of preeclamptic placentas. Pan-mammalian comparative analysis identified DLX5 as part of the human-specific regulatory network of trophoblast differentiation. Conclusions: Our analysis provides evidence of a true association among disturbed imprinting, gene expression, and preeclampsia. As a result of disturbed imprinting, the upregulated DLX5 affects trophoblast proliferation. Our in vitro model might fill a vital niche in preeclampsia research. Human-specific regulatory circuitry of DLX5 might help explain certain aspects of preeclampsia.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.117.028110
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
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  • 6
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    Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy
    Wiley ; 2017
    In:  American Journal of Reproductive Immunology Vol. 78, No. 5 ( 2017-11)
    Details
    In: American Journal of Reproductive Immunology, Wiley, Vol. 78, No. 5 ( 2017-11)
    Abstract: Preeclampsia (PE) is associated with inflammation and decreased Treg cells and IL‐10. The reduced uterine perfusion pressure (RUPP) rat model of PE exhibits these characteristics, and we hypothesized that induction of endogenous Tregs by a specific stimulus (CD28 superagonistic monoclonal antibody) would reduce inflammation, vasoactive factors, and hypertension in RUPP rats. Method of study RUPP was performed at gestation day (GD) 14; CD28 superagonist was administered intraperitoneally GD15; GD18 carotid catheters were inserted, and GD19 MAP and pup weight, blood, and tissues were collected. Results MAP (mmHg) in NP rats was 99±5 and 122±2 in RUPPs and was 111±1 mmHg in RUPP+SA. Circulating Tregs were 6±2% in NP rats and 0.77±0.49% in RUPP rats but increased to 11± 3% in RUPP+SA rats. Circulating IL‐6 and IL‐2 were decreased while IL‐10 and TGF‐B were significantly increased in RUPP+SA compared to RUPP controls. Vasoactive pathways such as ET‐1, AT1‐AA, and ROS were all reduced in RUPP+SA compared to RUPP. Pup weight was 2.4±0.05 mg in NP and 1.94±0.062 mg in RUPP and increased to 2.1± 0.05 mg in RUPP+SA. Conclusion These data suggest that stimulating endogenous Tregs lower factors causing hypertension and can improve fetal weight in response to PE.
    Type of Medium: Online Resource
    ISSN: 1046-7408 , 1600-0897
    URL: Issue
    URL: Article
    DOI: 10.1111/aji.2017.78.issue-5
    DOI: 10.1111/aji.12724
    RVK:
    XA 20240
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2024667-5
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  • 7
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    Abstract 576: Relaxin Dit Not Improve Outcome In An Established Preeclamptic Transgenic Rodent Rat Model
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. suppl_1 ( 2014-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. suppl_1 ( 2014-09)
    Abstract: Preeclampsia affects 5% of pregnancies in industrialized nations and consists of hypertension and proteinuria and characterized by maternal endothelial dysfunction and excessive vascular inflammation starting after 20 weeks of gestation. It represents a major cause for fetal and maternal morbidity and mortality and is an established risk factor for subsequent cardiovascular disease. Relaxin is a peptide hormone secreted by the corpus luteum, circulating in maternal blood during pregnancy. Its administration leads to rapid and sustained vasodilation. We hypothesized that relaxin ameliorates symptoms of preeclampsia in an established rat model. We used rats transgenic for the human angiotensinogen (hAogen) gene and the human rennin (hRen) gene and crossed the strains to produce a model of preeclampsia in the dams. On gestational day 9, hAogen TGR dams (PE rat) were randomly assigned to 2 experimental groups: vehicle (20 mM sodium acetate, pH 5.0,) or relaxin, at a dose of 2 μg/h of relaxin by subcutaneous osmotic minipump (Alzet, Typ 2002) until day 21 of gestation. Mean blood pressure was continuously recorded by radiotelemetry and 24 hour urine samples were collected in metabolic cages at day 18 of gestation. Rats were killed at day 21 of gestation. The fetuses and organs were removed and weighed. Vehicle treated PE rats developed hypertension abruptly at gestational day 13 and had sustained hypertension. Relaxin treatment did not prevent the increase in blood pressure in the last third of pregnancy (MAP on day 16 of gestation: 151.1 ± 2.2 mmHg vehicle vs. 156.6 ± 1.3 mmHg relaxin). Proteinuria was not ameliorated by relaxin (14.6 ± 5.5 mg/d vehicle vs. 20.8 ± 3.8 mg/d relaxin treated group). The number of live fetuses was similar between the groups. In addition, reduced fetal and uteroplacental unit weights were unaffected by relaxin treatment. Furthermore, relaxin treatment had no influence on intra uterine growth restriction, measured by brain to liver ratio (0.795 ± 0.021 vehicle vs. 0.795 ± 0.016 relaxin). Our data demonstrate that relaxin did not ameliorate hypertension, proteinuria or IUGR in a transgenic rat model for preeclampsia.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.64.suppl_1.576
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 8
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    Abstract 290: Upregulation Of Regulatory T Cells Improves Fetal Development In Preeclamptic Rat Model But Has No Influence On Hypertension And Proteinuria.
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. suppl_1 ( 2014-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. suppl_1 ( 2014-09)
    Abstract: Preeclampsia is characterized by hypertension, proteinuria and often associated with intrauterine growth retardation. There is a growing body of evidence that immunological dysregulation, involving T-cells, is implicated in causing preeclampsia. Proper recognition of paternal antigens by regulatory T cells is essential for successful outcome of pregnancy. The aim of the study was to evaluate the effect of upregulating regulatory T cells in an established transgenic rat model for preeclampsia. Application of CD28-superagonistic antibody has been shown to effectively upregulate regulatory T cells. In the first protocol (treatment arm) we applied 1mg of CD28-superagonist or control antibody on day 11 and 15 of pregnancy. In the second protocol (prevention arm) the superagonist or control antibody was applied on day 1, 5 and 9 to improve placentation with an upregulation of regulatory T cells at implantation site. Superagonist increased regulatory T cells in circulation and placenta from 1.6 ± 0.2% of CD4-positive T cells to 18.9 ± 4.8% and from 2.61 ± 0.96% to 23.27 ± 7.64%, respectively. Blood pressure (152.1 ± 5.8 mmHg vs 155.1 ± 3.6 mmHg, measured by telemetry on day 16) and albuminuria (30.6 ± 15.1 mg/d vs 14.6 ± 5.5 mg/d) were similar in the superagonist or sham treated preeclamptic group for both protocols. Rats treated with CD28-superagonist, showed higher pup weight (2.66 ± 0.03 g vs 2.37 ± 0.05 g) in preventive protocol and (3.04 ± 0.04 g vs 2.54 ± 0.1 g) in the treatment protocol. Intrauterine growth restriction, calculated by brain to liver weight ratio, was also decreased by superagonist in both protocols (0.88 ± 0.03 vs 1.07 ± 0.03 for prevention strategy and 0.72 ± 0.02 vs 1.05 ± 0.07 for therapeutic protocol respectively). Induction of regulatory T cells in circulation and uteroplacental unit early and late in an established preeclamptic rat model had no influence on hypertension and proteinuria. However, it improved the fetal outcome by ameliorating intrauterine growth retardation substantially.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.64.suppl_1.290
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
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  • 9
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    Natural Killer Cell Reduction and Uteroplacental Vasculopathy
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 68, No. 4 ( 2016-10), p. 964-973
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 68, No. 4 ( 2016-10), p. 964-973
    Abstract: Uterine natural killer cells are important for uteroplacental development and pregnancy maintenance. Their role in pregnancy disorders, such as preeclampsia, is unknown. We reduced the number of natural killer cells by administering rabbit anti-asialo GM1 antiserum in an established rat preeclamptic model (female human angiotensinogen×male human renin) and evaluated the effects at the end of pregnancy (day 21), compared with preeclamptic control rats receiving normal rabbit serum. In 100% of the antiserum-treated, preeclamptic rats (7/7), we observed highly degenerated vessel cross sections in the mesometrial triangle at the end of pregnancy. This maternal uterine vasculopathy was characterized by a total absence of nucleated/living cells in the vessel wall and perivascularly and prominent presence of fibrosis. Furthermore, there were no endovascular trophoblast cells within the vessel lumen. In the control, normal rabbit serum–treated, preeclamptic rats, only 20% (1/5) of the animals displayed such vasculopathy. We confirmed the results in healthy pregnant wild-type rats: after anti-asialo GM1 treatment, 67% of maternal rats displayed vasculopathy at the end of pregnancy compared with 0% in rabbit serum–treated control rats. This vasculopathy was associated with a significantly lower fetal weight in wild-type rats and deterioration of fetal brain/liver weight ratio in preeclamptic rats. Anti-asialo GM1 application had no influence on maternal hypertension and albuminuria during pregnancy. Our results show a new role of natural killer cells during hypertensive pregnancy in maintaining vascular integrity. In normotensive pregnancy, this integrity seems important for fetal growth.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.116.07800
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
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  • 10
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    Vitamin D depletion does not affect key aspects of the preeclamptic phenotype in a transgenic rodent model for preeclampsia
    Elsevier BV ; 2016
    In:  Journal of the American Society of Hypertension Vol. 10, No. 7 ( 2016-07), p. 597-607.e1
    Details
    In: Journal of the American Society of Hypertension, Elsevier BV, Vol. 10, No. 7 ( 2016-07), p. 597-607.e1
    Type of Medium: Online Resource
    ISSN: 1933-1711
    URL: Article
    DOI: 10.1016/j.jash.2016.05.008
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
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