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16 results on '"Fontijn, R.D."'

2. Delayed Microvascular Shear Adaptation in Pulmonary Arterial Hypertension. Role of Platelet Endothelial Cell Adhesion Molecule-1 Cleavage

Author

Szulcek, R., Happe, C.M., Rol, N., Fontijn, R.D., Dickhoff, C., Hartemink, K.J., Grünberg, K., Tu, L., Timens, W., Nossent, G.D., Paul, M.A., Leyen, T.A., Horrevoets, A.J., Man, F.S. de, Guignabert, C., Yu, P.B., Vonk-Noordegraaf, A., Nieuw Amerongen, G.P. van, Bogaard, H.J., Szulcek, R., Happe, C.M., Rol, N., Fontijn, R.D., Dickhoff, C., Hartemink, K.J., Grünberg, K., Tu, L., Timens, W., Nossent, G.D., Paul, M.A., Leyen, T.A., Horrevoets, A.J., Man, F.S. de, Guignabert, C., Yu, P.B., Vonk-Noordegraaf, A., Nieuw Amerongen, G.P. van, and Bogaard, H.J.

Abstract

Item does not contain fulltext, RATIONALE: Altered pulmonary hemodynamics and fluid flow-induced high shear stress (HSS) are characteristic hallmarks in the pathogenesis of pulmonary arterial hypertension (PAH). However, the contribution of HSS to cellular and vascular alterations in PAH is unclear. OBJECTIVES: We hypothesize that failing shear adaptation is an essential part of the endothelial dysfunction in all forms of PAH and tested whether microvascular endothelial cells (MVECs) or pulmonary arterial endothelial cells (PAECs) from lungs of patients with PAH adapt to HSS and if the shear defect partakes in vascular remodeling in vivo. METHODS: PAH MVEC (n = 7) and PAH PAEC (n = 3) morphology, function, protein, and gene expressions were compared with control MVEC (n = 8) under static culture conditions and after 24, 72, and 120 hours of HSS. MEASUREMENTS AND MAIN RESULTS: PAH MVEC showed a significantly delayed morphological shear adaptation (P = 0.03) and evidence of cell injury at sites of nonuniform shear profiles that are critical loci for vascular remodeling in PAH. In clear contrast, PAEC isolated from the same PAH lungs showed no impairments. PAH MVEC gene expression and transcriptional shear activation were not altered but showed significant decreased protein levels (P = 0.02) and disturbed interendothelial localization of the shear sensor platelet endothelial cell adhesion molecule-1 (PECAM-1). The decreased PECAM-1 levels were caused by caspase-mediated cytoplasmic cleavage but not increased cell apoptosis. Caspase blockade stabilized PECAM-1 levels, restored endothelial shear responsiveness in vitro, and attenuated occlusive vascular remodeling in chronically hypoxic Sugen5416-treated rats modeling severe PAH. CONCLUSIONS: Delayed shear adaptation, which promotes shear-induced endothelial injury, is a newly identified dysfunction specific to the microvascular endothelium in PAH. The shear response is normalized on stabilization of PECAM-1, which reverses intimal remodeling in vivo.

Published
2016

4. Functional implications of endothelial cell genomics

Author

Fontijn, R.D., Horrevoets, A.J.G., Pannekoek, H., Horrevoets, Antonius, ICaR - Ischemia and repair, Horrevoets, Antonius J. G., Pannekoek, Hans, Medical Biochemistry, and Faculteit der Geneeskunde

Published
2008

5. Rosuvastatin reduces atherosclerosis development beyond and independent of its plasma cholesterol-lowering effect in APOE*3-Leiden transgenic mice: Evidence for antiinflammatory effects of rosuvastatin

Author

Kleemann, R., Princen, H.M.G., Emeis, J.J., Jukema, J.W., Fontijn, R.D., Horrevoets, A.J.G., Kooistra, T., and Havekes, L.M.

Subjects
Biomedical Research, Mouse, Arteriosclerosis, Monocyte chemotactic protein 1, Pyrimidine derivative, Anti-Inflammatory Agents, Apolipoprotein E3, Monocyte, Animal tissue, Monocytes, Mice, Cell adhesion molecule, Pathology, Lipoprotein, Aorta, Sulfonamides, Cell adhesion molecules, Cholesterol diet, Lipid, Lipids, Cholesterol blood level, Blood, Cholesterol, Apolipoprotein E3 (Leidein), Cytokines, lipids (amino acids, peptides, and proteins), Female, Apolipoprotein E, Animal cell, Lipoproteins, Immunology, Mice, Transgenic, Sulfonamide, Rosuvastatin, Hydroxymethylglutaryl coenzyme A reductase inhibitor, Apolipoproteins E, Antiinflammatory agent, Transgenic mouse, Genetics, Cell Adhesion, Animals, Animal model, Animal experiment, Amyloid A protein, Biology, Cytokine, Inflammation, Inhibitors, Tumor necrosis factor alpha, Macrophages, Fluorobenzene, Fibrinogen, Statine derivative, Nonhuman, Drug effect, Fluorobenzenes, Metabolism, Pyrimidines, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Controlled study, Nucleotide sequence, Aorta root
Abstract

Background - Statins can exert anti-inflammatory antiatherosclerotic effects through an anti-inflammatory action, independent of lowering cholesterol. We addressed the question whether the anti-inflammatory activities of statins can reduce atherosclerosis beyond the reduction achieved by cholesterol lowering per se. Methods and Results - Two groups of 20 female APOE*3-Leiden mice received either a high-cholesterol diet (HC) or a high-cholesterol diet supplemented with 0.005% (wt/wt) rosuvastatin (HC+R). The HC diet alone resulted in a plasma cholesterol concentration of 18.9±1.4 mmol/L, and administration of rosuvastatin lowered plasma cholesterol to 14.1±0.7 mmol/L. In a separate low-cholesterol (LC) control group, the dietary cholesterol intake was reduced, which resulted in plasma cholesterol levels that were comparable to the HC+R group (13.4±0.8 mmol/L). Atherosclerosis in the aortic root area was quantified after 24 weeks. As compared with the HC group, the LC group had a 62% (P

Published
2003

8. Monovalent nickel in hydrogenase from Chromatium vinosum

Author

van der Zwaan, J.W., Albracht, S.P.J., Fontijn, R.D., and Slater, E.C.

Abstract

Redox titrations with hydrogenase from Chromatium vinosumshow that its nickel ion can exist in 3, possibly 4, different redox states: the 3 +, 2 +, 1 + and possibly a zero valent state. The 1 + state is unstable: oxidation to Ni(II) occurs unless H 2gas is present. The Ni(I) coordination, but not that of Ni(III), is highly light sensitive. A photoreaction occurs on illumination. It is irreversible below 77 K, but reversible at 200 K. The rate of this photodissociation reaction in 2H 2O is nearly 6-times slower than in H 2O, indicating the breakage of a nickel-hydrogen bond. This forms the first evidence for an H atom in the direct coordination sphere of Ni in hydrogenase and for the involvement of this metal in the reaction with hydrogen.

Published
1985
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