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Dive into the research topics where Inge Vreeswijk-Baudoin is active.

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Featured researches published by Inge Vreeswijk-Baudoin.


PLOS ONE | 2013

Gaseous Hydrogen Sulfide Protects against Myocardial Ischemia-Reperfusion Injury in Mice Partially Independent from Hypometabolism

Pauline M. Snijder; Rudolf A. de Boer; Eelke M. Bos; Joost C. van den Born; Willem-Peter T. Ruifrok; Inge Vreeswijk-Baudoin; Marcory C. R. F. van Dijk; Jan-Luuk Hillebrands; Henri G. D. Leuvenink; Harry van Goor

Background Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H2S) is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant properties. We investigated whether gaseous H2S administration is protective in cardiac IRI and whether non-hypometabolic concentrations of H2S have similar protective properties. Methods Male C57BL/6 mice received a 0, 10, or 100 ppm H2S-N2 mixture starting 30 minutes prior to ischemia until 5 minutes pre-reperfusion. IRI was inflicted by temporary ligation of the left coronary artery for 30 minutes. High-resolution respirometry equipment was used to assess CO2-production and blood pressure was measured using internal transmitters. The effects of H2S were assessed by histological and molecular analysis. Results Treatment with 100 ppm H2S decreased CO2-production by 72%, blood pressure by 14% and heart rate by 25%, while treatment with 10 ppm H2S had no effects. At day 1 of reperfusion 10 ppm H2S showed no effect on necrosis, while treatment with 100 ppm H2S reduced necrosis by 62% (p<0.05). Seven days post-reperfusion, both 10 ppm (p<0.01) and 100 ppm (p<0.05) H2S showed a reduction in fibrosis compared to IRI animals. Both 10 ppm and 100 ppm H2S reduced granulocyte-influx by 43% (p<0.05) and 60% (p<0.001), respectively. At 7 days post-reperfusion both 10 and 100 ppm H2S reduced expression of fibronectin by 63% (p<0.05) and 67% (p<0.01) and ANP by 84% and 63% (p<0.05), respectively. Conclusions Gaseous administration of H2S is protective when administered during a cardiac ischemic insult. Although hypometabolism is restricted to small animals, we now showed that low non-hypometabolic concentrations of H2S also have protective properties in IRI. Since IRI is a frequent cause of myocardial damage during percutaneous coronary intervention and cardiac transplantation, H2S treatment might lead to novel therapeutical modalities.


European Journal of Heart Failure | 2010

Activation of liver X receptors with T0901317 attenuates cardiac hypertrophy in vivo

Irma Kuipers; Jiang Li; Inge Vreeswijk-Baudoin; Johan Koster; Pim van der Harst; Herman H. W. Silljé; Folkert Kuipers; Dirk J. van Veldhuisen; Wiek H. van Gilst; Rudolf A. de Boer

Liver X receptor (LXR) is a nuclear receptor regulating cholesterol metabolism. Liver X receptor has also been shown to exert anti‐proliferative and anti‐inflammatory properties. In this study, we evaluated the effect of LXR activation on cardiac hypertrophy in vitro and in vivo.


PLOS ONE | 2013

Atrial Remodeling Is Directly Related to End-Diastolic Left Ventricular Pressure in a Mouse Model of Ventricular Pressure Overload

Anne Margreet De Jong; Isabelle C. Van Gelder; Inge Vreeswijk-Baudoin; Megan V. Cannon; Wiek H. van Gilst; Alexander H. Maass

Background Atrial fibrillation (AF) is often preceded by underlying cardiac diseases causing ventricular pressure overload. Objective It was our aim to investigate the progression of atrial remodeling in a small animal model of ventricular pressure overload and its association with induction of AF. Methods Male mice were subjected to transverse aortic constriction (TAC) or sham operation. After four or eight weeks, echocardiographic measurements and hemodynamic measurements were made and AF induction was tested. The hearts were either fixed in formalin or ventricles and atria were separated, weighed and snap-frozen for RNA analysis. Results Four weeks of pressure overload induced ventricular hypertrophy and minor changes in the atria. After eight weeks a significant reduction in left ventricular function occurred, associated with significant atrial remodeling including increased atrial weight, a trend towards an increased left atrial cell diameter, atrial dilatation and increased expression of markers of hypertrophy and inflammation. Histologically, no fibrosis was found in the left atrium. But atrial gene expression related to fibrosis was increased. Minor changes related to electrical remodeling were observed. AF inducibility was not different between the groups. Left ventricular end diastolic pressures were increased and correlated with the severity of atrial remodeling but not with AF induction. Conclusion Permanent ventricular pressure overload by TAC induced atrial remodeling, including hypertrophy, dilatation and inflammation. The extent of atrial remodeling was directly related to LVEDP and not duration of TAC per se.


American Journal of Physiology-renal Physiology | 2015

Pharmacological inhibition of galectin-3 protects against hypertensive nephropathy

Anne-Roos S. Frenay; Lili Yu; A. Rogier van der Velde; Inge Vreeswijk-Baudoin; Natalia López-Andrés; Harry van Goor; Herman H. W. Silljé; Willem P.T. Ruifrok; Rudolf A. de Boer

Galectin-3 activation is involved in the pathogenesis of renal damage and fibrogenesis. Limited data are available to suggest that galectin-3-targeted intervention is a potential therapeutic candidate for the prevention of chronic kidney disease. Homozygous TGR(mREN)27 (REN2) rats develop severe high blood pressure (BP) and hypertensive end-organ damage, including nephropathy and heart failure. Male REN2 rats were treated with N-acetyllactosamine [galectin-3 inhibitor (Gal3i)] for 6 wk; untreated REN2 and Sprague-Dawley rats served as controls. We measured cardiac function with echocardiogram and invasive hemodynamics before termination. BP and proteinuria were measured at baseline and at 3 and 6 wk. Plasma creatinine was determined at 6 wk. Renal damage was assessed for focal glomerular sclerosis, glomerular desmin expression, glomerular and interstitial macrophages, kidney injury molecule-1 expression, and α-smooth muscle actin expression. Inflammatory cytokines and extracellular matrix proteinases were quantified by quantitative real-time PCR. Systolic BP was higher in control REN2 rats, with no effect of Gal3i treatment. Plasma creatinine and proteinuria were significantly increased in control REN2 rats; Gal3i treatment reduced both. Renal damage (focal glomerular sclerosis, desmin, interstitial macrophages, kidney injury molecule-1, α-smooth muscle actin, collagen type I, and collagen type III) was also improved by Gal3i. All inflammatory markers (CD68, IL-68, galectin-3, and monocyte chemoattractant protein-1) were elevated in control REN2 rats and attenuated by Gal3i. Markers of extracellular matrix turnover were marginally altered in untreated REN2 rats compared with Sprague-Dawley rats. In conclusion, galectin-3 inhibition attenuated hypertensive nephropathy, as indicated by reduced proteinuria, improved renal function, and decreased renal damage. Drugs binding to galectin-3 may be therapeutic candidates for the prevention of chronic kidney disease.


Cardiovascular Research | 2013

Suicidal erythrocyte death, eryptosis, as a novel mechanism in heart failure-associated anaemia

Hasan Mahmud; Willem P.T. Ruifrok; B. Daan Westenbrink; Megan V. Cannon; Inge Vreeswijk-Baudoin; Wiek H. van Gilst; Herman H. W. Silljé; Rudolf A. de Boer

AIMS Suicidal death of erythrocytes (eryptosis) is characterized by cell shrinkage and exposure of phosphatidylserine (PS) residues at the cell surface. Excessive eryptosis may lead to anaemia. We aimed to study the role of eryptosis in heart failure (HF)-associated anaemia. METHODS AND RESULTS We measured eryptosis in rodent models of HF. Typical measures of eryptosis including PS-exposure, increased intracellular Ca(2+) levels, and decreased cell volume were determined by flow cytometry. Transgenic REN2 rats displayed mild anaemia which was associated with a two-fold increase in erythrocyte PS-exposure when compared with Sprague Dawley (SD) control rats (P < 0.01). Upon stimulation with eryptotic triggers such as oxidative stress, hyperosmotic shock and energy depletion, eryptosis was more prominent in REN2 as shown by increased PS-exposure, cytosolic Ca(2+) influx, and cell shrinkage (P < 0.05 vs. SD). Increasing cytosolic Ca(2+) levels resulted in a stronger increase in PS-exposure in REN2 erythrocytes (P < 0.01 vs. SD). Accordingly, inhibition of Ca(2+) entry blunted the increased PS-exposure upon oxidative stress. The REN2 rats had significantly higher reticulocytes (REN2: 10.6 ± 2.3%; SD: 5.4 ± 0.1%; P < 0.05) and erythrocyte turnover was increased, indicated by increased clearance of eryptotic erythrocytes. Eryptosis was also increased in a rat model of hypertensive cardiac remodelling (uninephrectomized rats implanted with deoxycorticosterone acetate pellets), in mice after transverse aortic constriction, as well as in a small proof-of-concept study in human HF patients. CONCLUSION Eryptosis is increased during HF development and could contribute to HF-associated anaemia. Eryptosis may therefore become a novel target for therapy in HF-associated anaemia.


American Journal of Physiology-heart and Circulatory Physiology | 2016

Parental vitamin D deficiency during pregnancy is associated with increased blood pressure in offspring via Panx1 hypermethylation

Laura M. G. Meems; Hasan Mahmud; Hendrik Buikema; Jörg Tost; Sven Michel; Janny Takens; Rikst Nynke Verkaik-Schakel; Inge Vreeswijk-Baudoin; Irene Mateo Leach; Torsten Plösch; Rudolf A. de Boer

Vitamin D deficiency is one of the most common nutritional deficiencies worldwide. Maternal vitamin D deficiency is associated with increased susceptibility to hypertension in offspring, but the reasons for this remain unknown. The aim of this study was to determine if parental vitamin D deficiency leads to altered DNA methylation in offspring that may relate to hypertension. Male and female Sprague-Dawley rats were fed a standard or vitamin D-depleted diet. After 10 wk, nonsibling rats were mated. The conceived pups received standard chow. We observed an increased systolic and diastolic blood pressure in the offspring from depleted parents (F1-depl). Genome-wide methylation analyses in offspring identified hypermethylation of the promoter region of the Pannexin-1 (Panx1) gene in F1-depl rats. Panx1 encodes a hemichannel known to be involved in endothelial-dependent relaxation, and we demonstrated that in F1-depl rats the increase in blood pressure was associated with impaired endothelial relaxation of the large vessels, suggesting an underlying biological mechanism of increased blood pressure in children from parents with vitamin deficiency. Parental vitamin D deficiency is associated with epigenetic changes and increased blood pressure levels in offspring.


PLOS ONE | 2016

Inhibition of Interleukin-6 Receptor in a Murine Model of Myocardial Ischemia-Reperfusion

Minke H. T. Hartman; Inge Vreeswijk-Baudoin; Hilde E. Groot; Kees W. A. van de Kolk; Rudolf A. de Boer; Irene Mateo Leach; Rozemarijn Vliegenthart; Herman H. W. Silljé; Pim van der Harst

Background Interleukin-6 (IL-6) levels are upregulated in myocardial infarction. Recent data suggest a causal role of the IL-6 receptor (IL-6R) in coronary heart disease. We evaluated if IL-6R blockade by a monoclonal antibody (MR16-1) prevents the heart from adverse left ventricular remodeling in a mouse model of ischemia-reperfusion (I/R). Methods CJ57/BL6 mice underwent I/R injury (left coronary artery ligation for 45 minutes) or sham surgery, and thereafter received MR16-1 (2mg/mouse) 5 minutes before reperfusion and 0.5mg/mouse weekly during four weeks, or control IgG treatment. Cardiac Magnetic Resonance Imaging (CMR) and hemodynamic measurements were performed to determine cardiac function after four weeks. Results I/R caused left ventricular dilatation and a decrease in left ventricular ejection fraction (LVEF). However, LVEF was significantly lower in the MR16-1 treatment group compared to the IgG group (28±4% vs. 35±6%, p = 0.02; sham 45±6% vs. 43±4%, respectively; p = NS). Cardiac relaxation (assessed by dP/dT) was not significantly different between the MR16-1 and IgG groups. Also, no differences were observed in histological myocardial fibrosis, infarct size and myocyte hypertrophy between the groups. Conclusion Blockade of the IL-6R receptor by the monoclonal MR16-1 antibody for four weeks started directly after I/R injury did not prevent the process of cardiac remodeling in mice, but rather associated with a deterioration in the process of adverse cardiac remodeling.


Science Translational Medicine | 2017

Accumulation of 5-oxoproline in myocardial dysfunction and the protective effects of OPLAH

Atze van der Pol; Andres Gil; Herman H. W. Silljé; Jasper Tromp; Ekaterina S. Ovchinnikova; Inge Vreeswijk-Baudoin; Martijn Hoes; Ibrahim J. Domian; Bart van de Sluis; Jan M. van Deursen; Adriaan A. Voors; Dirk J. van Veldhuisen; Wiek H. van Gilst; Eugene Berezikov; Pim van der Harst; Rudolf A. de Boer; Rainer Bischoff; Peter van der Meer

OPLAH is cardioprotective for myocardial infarction, and its substrate 5-oxoproline is a putative circulating marker for heart failure. A fetal gene for heart failure One way the heart responds to cardiac injury is by reverting gene expression to developmental patterns. Van der Pol et al. discovered that Oplah, a gene encoding an enzyme that converts 5-oxoproline to glutamate as part of the γ-glutamyl cycle, was repressed in adult mouse hearts with heart failure. Depleting Oplah in cardiomyocytes increased 5-oxoproline and oxidative stress, and elevated 5-oxoproline in blood samples from patients with heart failure was associated with worse outcome. Overexpressing OPLAH protected mice from cardiac injury in models of heart failure, suggesting that OPLAH and other fetal-like genes could be therapeutic targets. In response to heart failure (HF), the heart reacts by repressing adult genes and expressing fetal genes, thereby returning to a more fetal-like gene profile. To identify genes involved in this process, we carried out transcriptional analysis on murine hearts at different stages of development and on hearts from adult mice with HF. Our screen identified Oplah, encoding for 5-oxoprolinase, a member of the γ-glutamyl cycle that functions by scavenging 5-oxoproline. OPLAH depletion occurred as a result of cardiac injury, leading to elevated 5-oxoproline and oxidative stress, whereas OPLAH overexpression improved cardiac function after ischemic injury. In HF patients, we observed elevated plasma 5-oxoproline, which was associated with a worse clinical outcome. Understanding and modulating fetal-like genes in the failing heart may lead to potential diagnostic, prognostic, and therapeutic options in HF.


PLOS ONE | 2014

Cardiac Function and Architecture Are Maintained in a Model of Cardiorestricted Overexpression of the Prorenin-Renin Receptor

Hasan Mahmud; Wellington M Candido; Linda van Genne; Inge Vreeswijk-Baudoin; Hongjuan Yu; Bart van de Sluis; Jan M. van Deursen; Wiek H. van Gilst; Herman H. W. Silljé; Rudolf A. de Boer

The (pro)renin-renin receptor, (P)RR has been claimed to be a novel element of the renin-angiotensin system (RAS). The function of (P)RR has been widely studied in renal and vascular pathology but the cardio-specific function of (P)RR has not been studied in detail. We therefore generated a transgenic mouse (Tg) with cardio-restricted (P)RR overexpression driven by the alpha-MHC promotor. The mRNA expression of (P)RR was ∼170-fold higher (P<0.001) and protein expression ∼5-fold higher (P<0.001) in hearts of Tg mice as compared to non-transgenic (wild type, Wt) littermates. This level of overexpression was not associated with spontaneous cardiac morphological or functional abnormalities in Tg mice. To assess whether (P)RR could play a role in cardiac hypertrophy, we infused ISO for 28 days, but this caused an equal degree of cardiac hypertrophy and fibrosis in Wt and Tg mice. In addition, ischemia-reperfusion injury was performed in Langendorff perfused isolated mouse hearts. We did not observe differences in parameters of cardiac function or damage between Wt and Tg mouse hearts under these conditions. Finally, we explored whether the hypoxia sensing response would be modulated by (P)RR using HeLa cells with and without (P)RR overexpression. We did not establish any effect of (P)RR on expression of genes associated with the hypoxic response. These results demonstrate that cardio-specific overexpression of (P)RR does not provoke phenotypical differences in the heart, and does not affect the hearts’ response to stress and injury. It is concluded that increased myocardial (P)RR expression is unlikely to have a major role in pathological cardiac remodeling.


Transplant International | 2011

PRESERVATION OF NORMAL MORPHOLOGY OF HUMAN LIVERS AFTER 24 HOURS OF HYPOTHERMIC MACHINE PERFUSION. A FIRST-IN-MAN STUDY

Pauline M. Snijder; Rudolf A. de Boer; Eelke M. Bos; Joost C. van den Born; Willem-Peter T. Ruifrok; Inge Vreeswijk-Baudoin; Marcory C. R. F. van Dijk; Henri G. D. Leuvenink; Harry van Goor

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Rudolf A. de Boer

University Medical Center Groningen

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Herman H. W. Silljé

University Medical Center Groningen

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Wiek H. van Gilst

University Medical Center Groningen

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Hasan Mahmud

University Medical Center Groningen

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Megan V. Cannon

University Medical Center Groningen

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Pim van der Harst

University Medical Center Groningen

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Harry van Goor

University Medical Center Groningen

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Hendrik Buikema

University Medical Center Groningen

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Janny Takens

University Medical Center Groningen

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Laura M. G. Meems

University Medical Center Groningen

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