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31 results on '"Van der Vlies, Pieter"'

2. Shared DNA methylation signatures in childhood allergy: The MeDALL study

Author

Xu, Cheng-Jian, Gruzieva, Olena, Qi, Cancan, Esplugues, Ana, Gehring, Ulrike, Bergström, Anna, Mason, Dan, Chatzi, Leda, Porta, Daniela, Lodrup Carlsen, Karin C., Baïz, Nour, Madore, Anne-Marie, Alenius, Harri, van Rijkom, Bianca, Jankipersadsing, Soesma A., van der Vlies, Pieter, Kull, Inger, van Hage, Marianne, Bustamante, Mariona, Lertxundi, Aitana, Torrent, Matias, Santorelli, Gillian, Fantini, Maria Pia, Hovland, Vegard, Pesce, Giancarlo, Fyhrquist, Nanna, Laatikainen, Tiina, Nawijn, Martijn C., Li, Yang, Wijmenga, Cisca, Netea, Mihai G., Bousquet, Jean, Anto, Josep M., Laprise, Catherine, Haahtela, Tari, Annesi-Maesano, Isabella, Carlsen, Kai-Håkon, Gori, Davide, Kogevinas, Manolis, Wright, John, Söderhäll, Cilla, Vonk, Judith M., Sunyer, Jordi, Melén, Erik, and Koppelman, Gerard H.

Published
2021
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3. DNA methylation in childhood asthma: an epigenome-wide meta-analysis

Author

Xu, Cheng-Jian, Söderhäll, Cilla, Bustamante, Mariona, Baïz, Nour, Gruzieva, Olena, Gehring, Ulrike, Mason, Dan, Chatzi, Leda, Basterrechea, Mikel, Llop, Sabrina, Torrent, Maties, Forastiere, Francesco, Fantini, Maria Pia, Carlsen, Karin C Lødrup, Haahtela, Tari, Morin, Andréanne, Kerkhof, Marjan, Merid, Simon Kebede, van Rijkom, Bianca, Jankipersadsing, Soesma A, Bonder, Marc Jan, Ballereau, Stephane, Vermeulen, Cornelis J, Aguirre-Gamboa, Raul, de Jongste, Johan C, Smit, Henriette A, Kumar, Ashish, Pershagen, Göran, Guerra, Stefano, Garcia-Aymerich, Judith, Greco, Dario, Reinius, Lovisa, McEachan, Rosemary R C, Azad, Raf, Hovland, Vegard, Mowinckel, Petter, Alenius, Harri, Fyhrquist, Nanna, Lemonnier, Nathanaël, Pellet, Johann, Auffray, Charles, van der Vlies, Pieter, van Diemen, Cleo C, Li, Yang, Wijmenga, Cisca, Netea, Mihai G, Moffatt, Miriam F, Cookson, William O C M, Anto, Josep M, Bousquet, Jean, Laatikainen, Tiina, Laprise, Catherine, Carlsen, Kai-Håkon, Gori, Davide, Porta, Daniela, Iñiguez, Carmen, Bilbao, Jose Ramon, Kogevinas, Manolis, Wright, John, Brunekreef, Bert, Kere, Juha, Nawijn, Martijn C, Annesi-Maesano, Isabella, Sunyer, Jordi, Melén, Erik, and Koppelman, Gerard H

Published
2018
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4. Genetic and epigenetic regulation of YKL-40 in childhood

Author

Guerra, Stefano, Melén, Erik, Sunyer, Jordi, Xu, Cheng-Jian, Lavi, Iris, Benet, Marta, Bustamante, Mariona, Carsin, Anne-Elie, Dobaño, Carlota, Guxens, Mònica, Tischer, Christina, Vrijheid, Martine, Kull, Inger, Bergström, Anna, Kumar, Ashish, Söderhäll, Cilla, Gehring, Ulrike, Dijkstra, Dorieke J., van der Vlies, Pieter, Wickman, Magnus, Bousquet, Jean, Postma, Dirkje S., Anto, Josep M., and Koppelman, Gerard H.

Published
2018
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6. DNA Methylation in Newborns and Maternal Smoking in Pregnancy: Genome-wide Consortium Meta-analysis

Author

Joubert, Bonnie R., Felix, Janine F., Yousefi, Paul, Bakulski, Kelly M., Just, Allan C., Breton, Carrie, Reese, Sarah E., Markunas, Christina A., Richmond, Rebecca C., Xu, Cheng-Jian, Küpers, Leanne K., Oh, Sam S., Hoyo, Cathrine, Gruzieva, Olena, Söderhäll, Cilla, Salas, Lucas A., Baïz, Nour, Zhang, Hongmei, Lepeule, Johanna, Ruiz, Carlos, Ligthart, Symen, Wang, Tianyuan, Taylor, Jack A., Duijts, Liesbeth, Sharp, Gemma C., Jankipersadsing, Soesma A., Nilsen, Roy M., Vaez, Ahmad, Fallin, M. Daniele, Hu, Donglei, Litonjua, Augusto A., Fuemmeler, Bernard F., Huen, Karen, Kere, Juha, Kull, Inger, Munthe-Kaas, Monica Cheng, Gehring, Ulrike, Bustamante, Mariona, Saurel-Coubizolles, Marie José, Quraishi, Bilal M., Ren, Jie, Tost, Jörg, Gonzalez, Juan R., Peters, Marjolein J., Håberg, Siri E., Xu, Zongli, van Meurs, Joyce B., Gaunt, Tom R., Kerkhof, Marjan, Corpeleijn, Eva, Feinberg, Andrew P., Eng, Celeste, Baccarelli, Andrea A., Benjamin Neelon, Sara E., Bradman, Asa, Merid, Simon Kebede, Bergström, Anna, Herceg, Zdenko, Hernandez-Vargas, Hector, Brunekreef, Bert, Pinart, Mariona, Heude, Barbara, Ewart, Susan, Yao, Jin, Lemonnier, Nathanaël, Franco, Oscar H., Wu, Michael C., Hofman, Albert, McArdle, Wendy, Van der Vlies, Pieter, Falahi, Fahimeh, Gillman, Matthew W., Barcellos, Lisa F., Kumar, Ashish, Wickman, Magnus, Guerra, Stefano, Charles, Marie-Aline, Holloway, John, Auffray, Charles, Tiemeier, Henning W., Smith, George Davey, Postma, Dirkje, Hivert, Marie-France, Eskenazi, Brenda, Vrijheid, Martine, Arshad, Hasan, Antó, Josep M., Dehghan, Abbas, Karmaus, Wilfried, Annesi-Maesano, Isabella, Sunyer, Jordi, Ghantous, Akram, Pershagen, Göran, Holland, Nina, Murphy, Susan K., DeMeo, Dawn L., Burchard, Esteban G., Ladd-Acosta, Christine, Snieder, Harold, Nystad, Wenche, Koppelman, Gerard H., Relton, Caroline L., Jaddoe, Vincent W.V., Wilcox, Allen, Melén, Erik, and London, Stephanie J.

Published
2016
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13. Wnt Signaling and Dupuytrenʼs Disease

Author

Dolmans, Guido H., Werker, Paul M., Hennies, Hans C., Furniss, Dominic, Festen, Eleonora A., Franke, Lude, Becker, Kerstin, van der Vlies, Pieter, Wolffenbuttel, Bruce H., Tinschert, Sigrid, Toliat, Mohammad R., Nothnagel, Michael, Franke, Andre, Klopp, Norman, Wichmann, H.-Erich, Nürnberg, Peter, Giele, Henk, Ophoff, Roel A., and Wijmenga, Cisca

Published
2011
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15. A DGGE System for Comprehensive Mutation Screening of BRCA1 and BRCA2:: Application in a Dutch Cancer Clinic Setting

Author

van der Hout, Annemarie H., van den Ouweland, Ans M.W., van der Luijt, Rob B., Gille, Hans J.P., Bodmer, Daniëlle, Brüggenwirth, Hennie, Mulder, Inge M., van der Vlies, Pieter, Elfferich, Peter, Huisman, Maarten T., ten Berge, Annelies M., Kromosoeto, Joan, Jansen, Rumo P.M., van Zon, Patrick H.A., Vriesman, Thyrsa, Arts, Neeltje, Boutmy-de Lange, Majella, Oosterwijk, Jan C., Meijers-Heijboer, Hanne, Ausems, Margreet G.E.M., Hoogerbrugge, Nicoline, Verhoef, Senno, Halley, Dicky J.J., Vos, Yvonne J., Hogervorst, Frans, Ligtenberg, Marjolijn, and Hofstra, Robert M.W.

Published
2006
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20. Running‐wheel activity delays mitochondrial respiratory flux decline in aging mouse muscle via a post‐transcriptional mechanism.

Author

Stolle, Sarah, Ciapaite, Jolita, Reijne, Aaffien C., Talarovicova, Alzbeta, Wolters, Justina C., Aguirre‐Gamboa, Raúl, van der Vlies, Pieter, de Lange, Kim, Neerincx, Pieter B., van der Vries, Gerben, Deelen, Patrick, Swertz, Morris A., Li, Yang, Bischoff, Rainer, Permentier, Hjalmar P., Horvatovitch, Peter L., Groen, Albert K., van Dijk, Gertjan, Reijngoud, Dirk‐Jan, and Bakker, Barbara M.

Subjects
MITOCHONDRIAL pathology, SKELETAL muscle, EXERCISE physiology, MUSCLE metabolism, MUSCLE weakness, DISEASES
Abstract

Summary: Loss of mitochondrial respiratory flux is a hallmark of skeletal muscle aging, contributing to a progressive decline of muscle strength. Endurance exercise alleviates the decrease in respiratory flux, both in humans and in rodents. Here, we dissect the underlying mechanism of mitochondrial flux decline by integrated analysis of the molecular network. Mice were given a lifelong ad libitum low‐fat or high‐fat sucrose diet and were further divided into sedentary and running‐wheel groups. At 6, 12, 18 and 24 months, muscle weight, triglyceride content and mitochondrial respiratory flux were analysed. Subsequently, transcriptome was measured by RNA‐Seq and proteome by targeted LC‐MS/MS analysis with 13C‐labelled standards. In the sedentary groups, mitochondrial respiratory flux declined with age. Voluntary running protected the mitochondrial respiratory flux until 18 months of age. Beyond this time point, all groups converged. Regulation Analysis of flux, proteome and transcriptome showed that the decline of flux was equally regulated at the proteomic and at the metabolic level, while regulation at the transcriptional level was marginal. Proteomic regulation was most prominent at the beginning and at the end of the pathway, namely at the pyruvate dehydrogenase complex and at the synthesis and transport of ATP. Further proteomic regulation was scattered across the entire pathway, revealing an effective multisite regulation. Finally, reactions regulated at the protein level were highly overlapping between the four experimental groups, suggesting a common, post‐transcriptional mechanism of muscle aging. [ABSTRACT FROM AUTHOR]

Published
2018
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21. The emerging landscape of dynamic DNA methylation in early childhood.

Author

Cheng-Jian Xu, Bonder, Marc Jan, Söderhäll, Cilla, Bustamante, Mariona, Baïz, Nour, Gehring, Ulrike, Jankipersadsing, Soesma A., van der Vlies, Pieter, van Diemen, Cleo C., van Rijkom, Bianca, Just, Jocelyne, Kull, Inger, Kere, Juha, Antó, Josep Maria, Bousquet, Jean, Zhernakova, Alexandra, Wijmenga, Cisca, Annesi-Maesano, Isabella, Sunyer, Jordi, and Melén, Erik

Subjects
DNA methylation, GENETIC transcription, GENE expression, PHYSIOLOGICAL effects of tobacco, EPIGENETICS, CHILD development
Abstract

Background: DNA methylation has been found to associate with disease, aging and environmental exposure, but it is unknown how genome, environment and disease influence DNA methylation dynamics in childhood. Results: By analysing 538 paired DNA blood samples from children at birth and at 4-5 years old and 726 paired samples from children at 4 and 8 years old from four European birth cohorts using the Illumina Infinium Human Methylation 450 k chip, we have identified 14,150 consistent age-differential methylation sites (a-DMSs) at epigenomewide significance of p <1.14 x 10-7. Genes with an increase in age-differential methylation were enriched in pathways related to 'development', and were more often located in bivalent transcription start site (TSS) regions, which can silence or activate expression of developmental genes. Genes with a decrease in age-differential methylation were involved in cell signalling, and enriched on H3K27ac, which can predict developmental state. Maternal smoking tended to decrease methylation levels at the identified da-DMSs. We also found 101 a-DMSs (0.71%) that were regulated by genetic variants using cis-differential Methylation Quantitative Trait Locus (cis-dMeQTL) mapping. Moreover, a-DMS-associated genes during early development were significantly more likely to be linked with disease. Conclusion: Our study provides new insights into the dynamic epigenetic landscape of the first 8 years of life. [ABSTRACT FROM AUTHOR]

Published
2017
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22. RNA Sequencing Analysis of Intracranial Aneurysm Walls Reveals Involvement of Lysosomes and Immunoglobulins in Rupture.

Author

Kleinloog, Rachel, Verweij, Bon H., van der Vlies, Pieter, Deelen, Patrick, Swertz, Morris A., de Muynck, Louis, Van Damme, Philip, Giuliani, Fabrizio, Regli, Luca, van der Zwan, Albert, Berkelbach van der Sprenkel, Jan W., Han, K. Sen, Gosselaar, Peter, van Rijen, Peter C., Korkmaz, Emine, Post, Jan A., Rinkel, Gabriel J.E., Veldink, Jan H., and Ruigrok, Ynte M.

Published
2016
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23. Whole Blood Gene Expression Profiles of Patients with a Past Aneurysmal Subarachnoid Hemorrhage.

Author

van ’t Hof, Femke N. G., Ruigrok, Ynte M., Medic, Jelena, Sanjabi, Bahram, van der Vlies, Pieter, Rinkel, Gabriel J. E., and Veldink, Jan H.

Subjects
GENE expression, BLOOD testing, SUBARACHNOID hemorrhage, BIOMARKERS, COMPARATIVE studies, PATIENTS
Abstract

Background: The pathogenesis of development and rupture of intracranial aneurysms (IA) is largely unknown. Also, screening for IA to prevent aneurysmal subarachnoid hemorrhage (aSAH) is inefficient, as disease markers are lacking. We investigated gene expression profiles in blood of previous aSAH patients, who are still at risk for future IA, aiming to gain insight into the pathogenesis of IA and aSAH, and to make a first step towards improvement of aSAH risk prediction. Methods and Results: We collected peripheral blood of 119 patients with aSAH at least two years prior, and 118 controls. We determined gene expression profiles using Illumina HumanHT-12v4 BeadChips. After quality control, we divided the dataset in a discovery (2/3) and replication set (1/3), identified differentially expressed genes, and applied (co-)differential co-expression to identify disease-related gene networks. No genes with a significant (false-discovery rate <5%) differential expression were observed. We detected one gene network with significant differential co-expression, but did not find biologically meaningful gene networks related to a history of aSAH. Next, we applied prediction analysis of microarrays to find a gene set that optimally predicts absence or presence of a history of aSAH. We found no gene sets with a correct disease state prediction higher than 40%. Conclusions: No gene expression differences were present in blood of previous aSAH patients compared to controls, besides one differentially co-expressed gene network without a clear relevant biological function. Our findings suggest that gene expression profiles, as detected in blood of previous aSAH patients, do not reveal the pathogenesis of IA and aSAH, and cannot be used for aSAH risk prediction. [ABSTRACT FROM AUTHOR]

Published
2015
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26. Lessons Learned from Whole Exome Sequencing in Multiplex Families Affected by a Complex Genetic Disorder, Intracranial Aneurysm.

Author

Farlow, Janice L., Lin, Hai, Sauerbeck, Laura, Lai, Dongbing, Koller, Daniel L., Pugh, Elizabeth, Hetrick, Kurt, Ling, Hua, Kleinloog, Rachel, van der Vlies, Pieter, Deelen, Patrick, Swertz, Morris A., Verweij, Bon H., Regli, Luca, Rinkel, Gabriel J. E., Ruigrok, Ynte M., Doheny, Kimberly, Liu, Yunlong, Broderick, Joseph, and Foroud, Tatiana

Subjects
NUCLEOTIDE sequence, GENETIC disorders, INTRACRANIAL aneurysms, DISEASE susceptibility, GENE expression, GENETICS, DISEASE risk factors
Abstract

Genetic risk factors for intracranial aneurysm (IA) are not yet fully understood. Genomewide association studies have been successful at identifying common variants; however, the role of rare variation in IA susceptibility has not been fully explored. In this study, we report the use of whole exome sequencing (WES) in seven densely-affected families (45 individuals) recruited as part of the Familial Intracranial Aneurysm study. WES variants were prioritized by functional prediction, frequency, predicted pathogenicity, and segregation within families. Using these criteria, 68 variants in 68 genes were prioritized across the seven families. Of the genes that were expressed in IA tissue, one gene (TMEM132B) was differentially expressed in aneurysmal samples (n=44) as compared to control samples (n=16) (false discovery rate adjusted p-value=0.023). We demonstrate that sequencing of densely affected families permits exploration of the role of rare variants in a relatively common disease such as IA, although there are important study design considerations for applying sequencing to complex disorders. In this study, we explore methods of WES variant prioritization, including the incorporation of unaffected individuals, multipoint linkage analysis, biological pathway information, and transcriptome profiling. Further studies are needed to validate and characterize the set of variants and genes identified in this study. [ABSTRACT FROM AUTHOR]

Published
2015
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27. Global correlation of genome and transcriptome changes in classical Hodgkin lymphoma.

Author

Kluiver, Joost, Kok, Klaas, Pfeil, Ines, de Jong, Debora, Blokzijl, Tjasso, Harms, Geert, van der Vlies, Pieter, Diepstra, Arjan, Atayar, Çiğdem, Poppema, Sibrand, Küppers, Ralf, and van den Berg, Anke

Abstract

To identify genes involved in the pathogenesis of classical Hodgkin lymphoma (cHL), we performed serial analysis of gene expression (SAGE) and array-based comparative genomic hybridization (aCGH). Comparison of SAGE libraries of cHL cell lines L428 and L1236 with that of germinal centre B cells revealed consistent overexpression of only 14 genes. In contrast, 141 genes were downregulated in both cHL cell lines, including many B cell and HLA genes. aCGH revealed gain of 2p, 7p, 9p, 11q and Xq and loss of 4q and 11q. Eighteen percent of the differentially expressed genes mapped to regions with loss or gain and a good correlation was observed between underexpression and loss or overexpression and gain of DNA. Remarkably, gain of 2p and 9p did not correlate with increased expression of the proposed target genes c-REL and JAK2. Downregulation of many genes within the HLA region also did not correlate with loss of DNA. FSCN1 and IRAK1 mapping at genomic loci (7p and Xq) that frequently showed gain were overexpressed in cHL cell lines and might be involved in the pathogenesis of cHL. Copyright © 2006 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2007
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29. Transcriptome analysis suggests a compensatory role of the cofactors coenzyme A and NAD+ in medium-chain acyl-CoA dehydrogenase knockout mice.

Author

Martines, Anne-Claire M. F., Gerding, Albert, Stolle, Sarah, Vieira-Lara, Marcel A., Wolters, Justina C., Jurdzinski, Angelika, Bongiovanni, Laura, de Bruin, Alain, van der Vlies, Pieter, van der Vries, Gerben, Bloks, Vincent W., Derks, Terry G. J., Reijngoud, Dirk-Jan, and Bakker, Barbara M.

Subjects
TRANSCRIPTOMES, COENZYME A, DEHYDROGENASES, ENZYME deficiency, LABORATORY mice
Abstract

During fasting, mitochondrial fatty-acid β-oxidation (mFAO) is essential for the generation of glucose by the liver. Children with a loss-of-function deficiency in the mFAO enzyme medium-chain acyl-Coenzyme A dehydrogenase (MCAD) are at serious risk of life-threatening low blood glucose levels during fasting in combination with intercurrent disease. However, a subset of these children remains asymptomatic throughout life. In MCAD-deficient (MCAD-KO) mice, glucose levels are similar to those of wild-type (WT) mice, even during fasting. We investigated if metabolic adaptations in the liver may underlie the robustness of this KO mouse. WT and KO mice were given a high- or low-fat diet and subsequently fasted. We analyzed histology, mitochondrial function, targeted mitochondrial proteomics, and transcriptome in liver tissue. Loss of MCAD led to a decreased capacity to oxidize octanoyl-CoA. This was not compensated for by altered protein levels of the short- and long-chain isoenzymes SCAD and LCAD. In the transcriptome, we identified subtle adaptations in the expression of genes encoding enzymes catalyzing CoA- and NAD(P)(H)-involving reactions and of genes involved in detoxification mechanisms. We discuss how these processes may contribute to robustness in MCAD-KO mice and potentially also in asymptomatic human subjects with a complete loss of MCAD activity. [ABSTRACT FROM AUTHOR]

Published
2019
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30. Improvements in gel composition and electrophoretic conditions for broad-range mutation analysis by denaturing gradient gel electrophoresis.

Author

Hayes, Vanessa M., Wu, Ying, Osinga, Jan, Mulder, Inge M., van der Vlies, Pieter, Elfferich, Peter, Buys, Charles H. C. M., Hofstra, Robert M. W., Fischer, S.G., Sheffield, V.C., Abrams, E.S., Lerman, L.S., Wu, Y., Guldberg, P., van Orsouw, N.J., Michiels, L., Traystman, M.D., Hayes, V.M., Myers, R.M., and Gelfi, C.

Published
1999
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