A. M. Van der Laan
University of Amsterdam
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Featured researches published by A. M. Van der Laan.
Netherlands Heart Journal | 2008
A. M. Van der Laan; Alexander Hirsch; Robin Nijveldt; P. A. van der Vleuten; W.J. van der Giessen; P. A. Doevendans; Johannes Waltenberger; J. M. ten Berg; W.R.M. Aengevaeren; Jaap Jan Zwaginga; Bart J. Biemond; A. C. Van Rossum; J. G. P. Tijssen; F. Zijlstra; Jan J. Piek
AbstractDuring the last decennium, the role of bone marrow mononuclear cells (BMMC) has been underscored in the healing process after acute myocardial infarction (AMI). Although these cells improve left ventricular recovery after AMI in experimental studies, results from large-scale randomised trials investigating BMMC therapy in patients with AMI have shown contradictory results. To address this issue the HEBE study was designed, a multicentre, randomised trial, evaluating the effects of intracoronary infusion of BMMCs and the effects of intracoronary infusion of peripheral blood mononuclear cells after primary percutaneous coronary intervention. The primary endpoint of the HEBE trial is the change in regional myocardial function in dysfunctional segments at four months relative to baseline, based on segmental analysis as measured by magnetic resonance imaging. The results from the HEBE trial will provide detailed information about the effects of intracoronary BMMC therapy on post-infarct left ventricular recovery. In addition, further analysis of the data and material obtained may provide important mechanistic insights into the contribution of BMMCs to natural recovery from AMI as well as the response to cell therapy. This may significantly contribute to the development of improved cell-based therapies, aiming at optimising post-infarct recovery and preventing heart failure. (Neth Heart J 2008;16:436-9.)
Heart | 2013
N.W. Van Der Hoeven; P.F.A. Teunissen; Gerald S. Werner; Ronak Delewi; Stephan H. Schirmer; Tobias Traupe; A. M. Van der Laan; J. G. P. Tijssen; Jan J. Piek; Christian Seiler; N. van Royen
Objective Well-developed collaterals provide survival benefit in patients with obstructive coronary artery disease (CAD). Therefore, in this study we sought to determine which clinical variables are associated with arteriogenesis. Design Clinical and laboratory variables were collected before percutaneous coronary intervention. Multivariate analysis was performed to determine which variables are associated with the collateral flow index (CFI). Patients Data from 295 chronic total occlusion (CTO) patients (Bern, Switzerland, Amsterdam, the Netherlands and Jena, Germany) were pooled. In earlier studies, patients had varying degrees of stenosis. Therefore, different stages of development of the collaterals were used. In our study, a unique group of patients with CTO was analysed. Interventions Instead of angiography used earlier, we used a more accurate method to determine CFI using intracoronary pressure measurements. CFI was calculated from the occlusive pressure distal of the coronary lesion, the aortic pressure and central venous pressure. Results The mean CFI was 0.39±0.14. After multivariate analysis, β blockers, hypertension and angina pectoris duration were positively associated with CFI (B: correlation coefficient β=0.07, SE=0.03, p=0.02, B=0.040, SE=0.02, p=0.042 and B=0.001, SE=0.000, p=0.02). Furthermore also after multivariate analysis, high serum leucocytes, prior myocardial infarction and high diastolic blood pressure were negatively associated with CFI (B=−0.01, SE=0.005, p=0.03, B=−0.04, SE=0.02, p=0.03 and B=−0.002, SE=0.001, p=0.011). Conclusions In this unique cohort, high serum leucocytes and high diastolic blood pressure are associated with poorly developed collaterals. Interestingly, the use of β blockers is associated with well-developed collaterals, shedding new light on the potential action mode of this drug in patients with CAD.
Journal of Biological Chemistry | 2010
Stephan H. Schirmer; Pieter T. Bot; Joost O. Fledderus; A. M. Van der Laan; Oscar L. Volger; Ulrich Laufs; Michael Böhm; Carlie J.M. de Vries; Anton J.G. Horrevoets; Jan J. Piek; Imo E. Hoefer; Niels van Royen
Increased interferon (IFN)-β signaling in patients with insufficient coronary collateralization and an inhibitory effect of IFNβ on collateral artery growth in mice have been reported. The mechanisms of IFNβ-induced inhibition of arteriogenesis are unknown. In stimulated monocytes from patients with chronic total coronary artery occlusion and decreased arteriogenic response, whole genome expression analysis showed increased expression of IFNβ-regulated genes. Immunohistochemically, the IFNβ receptor was localized in the vascular media of murine collateral arteries. Treatment of vascular smooth muscle cells (VSMC) with IFNβ resulted in an attenuated proliferation, cell-cycle arrest, and increased expression of cyclin-dependent kinase inhibitor-1A (p21). The growth inhibitory effect of IFNβ was attenuated by inhibition of p21 by RNA interference. IFNβ-treated THP1 monocytes showed enhanced apoptosis. Subsequently, we tested if collateral artery growth can be stimulated by inhibition of IFNβ-signaling. RNA interference of the IFNβ receptor-1 (IFNAR1) increased VSMC proliferation, cell cycle progression, and reduced p21 gene expression. IFNβ signaling and FAS and TRAIL expression were attenuated in monocytes from IFNAR1−/− mice, indicating reduced monocyte apoptosis. Hindlimb perfusion restoration 1 week after femoral artery ligation was improved in IFNAR1−/− mice compared with wild-type mice as assessed by infusion of fluorescent microspheres. These results demonstrate that IFNβ inhibits collateral artery growth and VSMC proliferation through p21-dependent cell cycle arrest and induction of monocyte apoptosis. Inhibition of IFNβ stimulates VSMC proliferation and collateral artery growth.
Vascular Pharmacology | 2012
T C T M van der Pouw Kraan; A. M. Van der Laan; Jan J. Piek; Anton J.G. Horrevoets
In this review we compare expression studies on monocyte subsets as an example to show the integrated possibilities of molecular databases and bioinformatic analysis tools. Monocytes have been recognized as cells with great plasticity and differentiation potential that play a pivotal role in revascularization processes, i.e. angiogenesis and arteriogenesis. To gain more insight in the relevant developmental programs, we compared the full-genome mRNA expression profiles of several distinct human monocyte subpopulations previously identified based on surface marker expression. These included classical and non-classical, M1 and M2 macrophages, circulating angiogenic cells (CAC), and non-monocyte-derived endothelial colony-forming cells (ECFC). Their transcriptional profiles revealed distinct and overlapping gene expression signatures and pathways reminiscent of utilization of transcription factors driving polarization into the different monocytic phenotypes. Hierarchical cluster analysis revealed that CAC are most related to M2 macrophages and unstimulated macrophages, and to a lesser extent to classical monocytes, and are quite distinct from M1 macrophages and ECFC. Analysis of the promoter region of CAC-expressed genes suggests that in particular the ETS family of transcription factors is important in CAC development. These analyses show the power of combining multiple datasets with existing databases on biological knowledge, to interpret full genome expression data.
European Heart Journal | 2011
Lourens Robbers; Robin Nijveldt; A. M. Van der Laan; R. Delewi; Alexander Hirsch; P. A. van der Vleuten; Aernout M. Beek; Jan J. Piek; F. Zijlstra; A. C. Van Rossum
European Heart Journal Supplements | 2010
Ronak Delewi; Robin Nijveldt; A. M. Van der Laan; Alexander Hirsch; P. A. van der Vleuten; Margriet I. Klees; J. G. P. Tijssen; F. Zijlstra; A. C. Van Rossum; Jan J. Piek
European Heart Journal | 2009
A. M. Van der Laan; P. A. van der Vleuten; Alexander Hirsch; Robin Nijveldt; W.J. van der Giessen; Bart J. Biemond; J. G. P. Tijssen; A. C. Van Rossum; F. Zijlstra; Jan J. Piek; Hebe Investigators
European Heart Journal Supplements | 2010
Ronak Delewi; Robin Nijveldt; H. de Bruin; Alexander Hirsch; A. M. Van der Laan; J. P. G. Tijssen; A. C. Van Rossum; F. Zijlstra; Jan J. Piek; Bonno N. Bouma
European Heart Journal | 2010
Ronak Delewi; A. M. Van der Laan; Robin Nijveldt; Alexander Hirsch; P. A. van der Vleuten; Margriet I. Klees; J. G. P. Tijssen; F. Zijlstra; A. C. Van Rossum; Jan J. Piek
Atherosclerosis Supplements | 2010
T C T M van der Pouw Kraan; Stephan H. Schirmer; Joost O. Fledderus; Perry D. Moerland; Thomas A. Leyen; A. M. Van der Laan; Jan J. Piek; N. van Royen; Anton J Horrevoets