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  • JOURNAL ARTICLE
    Olivon VC, Segers D, de Oliveira AM, Demougeot C, Bertholet A, de Crom R, Krams R, Stergiopulos N, da Silva RFet al., 2011,

    Effects of arginase inhibition on shear stress-induced plaque size and composition

    , EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Vol: 41, Pages: 6-6, ISSN: 0014-2972
  • JOURNAL ARTICLE
    Pedrigi RM, Simon D, Reed A, Stamer WD, Overby DRet al., 2011,

    A model of giant vacuole dynamics in human Schlemm's canal endothelial cells

    , EXPERIMENTAL EYE RESEARCH, Vol: 92, Pages: 57-66, ISSN: 0014-4835
  • JOURNAL ARTICLE
    Pfenniger A, Sutter E, Cuhlmann S, Evans PC, Krams R, Kwak BRet al., 2011,

    Endothelial Cx37 expression is regulated by the shear stress responsive transcription factor KLF2

    , EUROPEAN HEART JOURNAL, Vol: 32, Pages: 937-937, ISSN: 0195-668X
  • JOURNAL ARTICLE
    Poelma C, Mari JM, Foin N, Tang M-X, Krams R, Caro CG, Weinberg PD, Westerweel Jet al., 2011,

    3D Flow reconstruction using ultrasound PIV

    , EXPERIMENTS IN FLUIDS, Vol: 50, Pages: 777-785, ISSN: 0723-4864
  • JOURNAL ARTICLE
    Segers D, Lipton JA, Leenen PJM, Cheng C, Tempel D, Pasterkamp G, Moll FL, de Crom R, Krams Ret al., 2011,

    Atherosclerotic Plaque Stability Is Affected by the Chemokine CXCL10 in Both Mice and Humans.

    , Int J Inflam, Vol: 2011

    Background. The chemokine CXCL10 is specifically upregulated during experimental development of plaque with an unstable phenotype. In this study we evaluated the functional consequences of these findings in mice and humans. Methods and Results. In ApoE(-/-) mice, we induced unstable plaque with using a flow-altering device around the carotid artery. From week 1 to 4, mice were injected with a neutralizing CXCL10 antibody. After 9 weeks, CXCL10 inhibition resulted in a more stable plaque phenotype: collagen increased by 58% (P = 0.002), smooth muscle cell content increased 2-fold (P = 0.03), while macrophage MHC class II expression decreased by 50% (P = 0.005). Also, the size of necrotic cores decreased by 41% (P = 0.01). In 106 human carotid endarterectomy specimens we found that increasing concentrations of CXCL10 strongly associate with an increase in atheromatous plaque phenotype (ANOVA, P = 0.003), with high macrophage, low smooth muscle cell, and low collagen content. Conclusions. In the present study we showed that CXCL10 is associated with the development of vulnerable plaque in human and mice. We conclude that CXCL10 might provide a new lead towards plaque-stabilizing therapy.

  • JOURNAL ARTICLE
    Yla-Herttuala S, Bentzon JF, Daemen M, Falk E, Garcia-Garcia HM, Herrmann J, Hoefer I, Jukema JW, Krams R, Kwak BR, Marx N, Naruszewicz M, Newby A, Pasterkamp G, Serruys PWJC, Waltenberger J, Weber C, Tokgozoglu Let al., 2011,

    Stabilisation of atherosclerotic plaques Position Paper of the European Society of Cardiology (ESC) Working Group on Atherosclerosis and Vascular Biology

    , THROMBOSIS AND HAEMOSTASIS, Vol: 106, Pages: 1-19, ISSN: 0340-6245
  • JOURNAL ARTICLE
    Zakkar M, Luong LA, Chaudhury H, Ruud O, Punjabi PP, Anderson JR, Mullholand JW, Clements AT, Krams R, Foin N, Athanasiou T, Leen ELS, Mason JC, Haskard DO, Evans PCet al., 2011,

    Dexamethasone Arterializes Venous Endothelial Cells by Inducing Mitogen-Activated Protein Kinase Phosphatase-1 A Novel Antiinflammatory Treatment for Vein Grafts?

    , CIRCULATION, Vol: 123, Pages: 524-U141, ISSN: 0009-7322
  • JOURNAL ARTICLE
    van Bochove GS, Paulis LEM, Segers D, Mulder WJM, Krams R, Nicolay K, Strijkers GJet al., 2011,

    Contrast enhancement by differently sized paramagnetic MRI contrast agents in mice with two phenotypes of atherosclerotic plaque

    , CONTRAST MEDIA & MOLECULAR IMAGING, Vol: 6, Pages: 35-45, ISSN: 1555-4309
  • JOURNAL ARTICLE
    Chaudhury H, Zakkar M, Boyle J, Cuhlmann S, van der Heiden K, Luong LA, Davis J, Platt A, Mason JC, Krams R, Haskard DO, Clark AR, Evans PCet al., 2010,

    c-Jun N-Terminal Kinase Primes Endothelial Cells at Atheroprone Sites for Apoptosis

    , ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 30, Pages: 546-U393, ISSN: 1079-5642
  • JOURNAL ARTICLE
    Da Silva RF, Olivon VC, Segers D, De Crom R, Krams R, Stergiopuloss Net al., 2010,

    Ex vivo and in vivo regulation of arginase in response to wall shear stress

    , IFMBE Proceedings, Vol: 29, Pages: 753-756, ISSN: 1680-0737

    Background: Alterations of wall shear stress can predispose the endothelium to the development of atherosclerotic plaques. We evaluated the modulation of arginase by wall shear stress. Material and methods: We perfused isolated carotid arterial segments to either unidirectional high mean shear stress (HSS) or low mean and oscillating shear stress (OSS) for 3 days. Vascular function was analyzed by diameter measurement, arginase expression and localization by western blot and immunohistochemistry, respectively. These effects were also evaluated in right carotid artery of apolipoprotein E (apoE-/-) deficient mice, fed with high cholesterol diet, which was exposed to HSS, LSS and OSS flow conditions by the placement of a shear stress modifier for 9 weeks. ApoE-/- mice received either the arginase inhibitor nor-Noha (20mg/kg, 5 days/week) or placebo for 9 weeks. Plaque size and I/M ratio were determined by histology. Results: Our data from ex vivo perfusion showed that exposure of carotid segments to both low and oscillatory flow conditions significantly increase arginase II protein expression and activity as compared to high shear stress athero-protective flow condition. Long-term treatment with nor-Noha effectively decreased arginase activity at LSS and OSS regions, which in turn was accompanied by a decreased I/M ratio and the size of atherosclerotic lesion. In the lesion, inhibition of arginase decreased the number of CD68 positive cells at LSS and OSS zones. Exposure of carotid artery to OSS induced a more pronounced activation of arginase as compared to HSS. Conclusions: Arginase is modulated by patterns of wall shear stress. Long-term treatment of apoE- /- mice with arginase inhibitor decreased carotid I/M ratio and atherosclerotic lesion at LSS and OSS regions. Therefore, inhibition of arginase by nor-Noha may emerge as a distinct way to target atherosclerosis disease. © 2010 International Federation for Medical and Biological Engineering.

  • BOOK CHAPTER
    Deac F, Cotolan N, Kis Z, Silaghi-Dumitrescu Ret al., 2010,

    A dithionite-induced six-coordinated species at the heme in deoxy-hemoglobin

    , Metal Elements in Environment, Medicine and Biology Tome X, Editors: Garban, Silaghi-Dumitrescu, Sayti, Romania, Timisoara, Publisher: Eurobit Publishing House
  • JOURNAL ARTICLE
    Debernardi N, Roijers RB, Krams R, de Crom R, Mutsaers PHA, van der Vusse GJet al., 2010,

    Microcalcifications in atherosclerotic lesion of apolipoprotein E-deficient mouse

    , INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Vol: 91, Pages: 485-494, ISSN: 0959-9673
  • JOURNAL ARTICLE
    Friedman MH, Krams R, Chandran KB, 2010,

    Flow Interactions with Cells and Tissues: Cardiovascular Flows and Fluid-Structure Interactions

    , ANNALS OF BIOMEDICAL ENGINEERING, Vol: 38, Pages: 1178-1187, ISSN: 0090-6964
  • JOURNAL ARTICLE
    Friedman MH, Krams R, Chandran KB, 2010,

    Flow interactions with cells and tissues: cardiovascular flows and fluid-structure interactions. Sixth International Bio-Fluid Mechanics Symposium and Workshop, March 28-30, 2008, Pasadena, California.

    , Ann Biomed Eng, Vol: 38, Pages: 1178-1187

    Interactions between flow and biological cells and tissues are intrinsic to the circulatory, respiratory, digestive and genitourinary systems. In the circulatory system, an understanding of the complex interaction between the arterial wall (a living multi-component organ with anisotropic, nonlinear material properties) and blood (a shear-thinning fluid with 45% by volume consisting of red blood cells, platelets, and white blood cells) is vital to our understanding of the physiology of the human circulation and the etiology and development of arterial diseases, and to the design and development of prosthetic implants and tissue-engineered substitutes. Similarly, an understanding of the complex dynamics of flow past native human heart valves and the effect of that flow on the valvular tissue is necessary to elucidate the etiology of valvular diseases and in the design and development of valve replacements. In this paper we address the influence of biomechanical factors on the arterial circulation. The first part presents our current understanding of the impact of blood flow on the arterial wall at the cellular level and the relationship between flow-induced stresses and the etiology of atherosclerosis. The second part describes recent advances in the application of fluid-structure interaction analysis to arterial flows and the dynamics of heart valves.

  • JOURNAL ARTICLE
    Helderman F, Manoch IJ, Breeuwer M, Kose U, Boersma H, van Sambeek MRHM, Pattynama PMT, Schouten O, Poldermans D, Wisselink W, van der Steen AFW, Krams Ret al., 2010,

    Predicting Patient-Specific Expansion of Abdominal Aortic Aneurysms

    , EUROPEAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY, Vol: 40, Pages: 47-53, ISSN: 1078-5884

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