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419 results on '"Niessen, Hans W. M."'

1. Bone marrow adipocytes fuel emergency hematopoiesis after myocardial infarction

Author

Zhang, Shuang, Paccalet, Alexandre, Rohde, David, Cremer, Sebastian, Hulsmans, Maarten, Lee, I-Hsiu, Mentkowski, Kyle, Grune, Jana, Schloss, Maximilian J., Honold, Lisa, Iwamoto, Yoshiko, Zheng, Yi, Bredella, Miriam A., Buckless, Colleen, Ghoshhajra, Brian, Thondapu, Vikas, van der Laan, Anja M., Piek, Jan J., Niessen, Hans W. M., Pallante, Fabio, Carnevale, Raimondo, Perrotta, Sara, Carnevale, Daniela, Iborra-Egea, Oriol, Muñoz-Guijosa, Christian, Galvez-Monton, Carolina, Bayes-Genis, Antoni, Vidoudez, Charles, Trauger, Sunia A., Scadden, David T., Swirski, Filip K., Moskowitz, Michael A., Naxerova, Kamila, and Nahrendorf, Matthias

Published
2023
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4. Atrial epicardial adipose tissue abundantly secretes myeloperoxidase and activates atrial fibroblasts in patients with atrial fibrillation

Author

Meulendijks, Eva R., Al-Shama, Rushd F. M., Kawasaki, Makiri, Fabrizi, Benedetta, Neefs, Jolien, Wesselink, Robin, Ernault, Auriane C., Piersma, Sander, Pham, Thang V., Jimenez, Connie R., Knol, Jaco C., van Boven, Wim J. P., Driessen, Antoine H. G., de Vries, Tim A. C., van der Leeden, Britt, Niessen, Hans W. M., de Boer, Onno J., Krul, S. bastien P. J., de Groot, Joris R., Cardiology, Experimental Cardiology, ACS - Heart failure & arrhythmias, Cardiothoracic Surgery, ACS - Pulmonary hypertension & thrombosis, and Pathology

Abstract

Background: Epicardial adipose tissue (EAT) secretome induces fibrosis. Fibrosis, primarily extracellular matrix (ECM) produced by fibroblasts, creates a substrate for atrial fibrillation (AF). Whether the EAT secretome from patients with AF activates human atrial fibroblasts and through which components, remains unexplored. Research aims: (a) To investigate if the EAT secretome from patients with versus without AF increases ECM production in atrial fibroblasts. (b) To identify profibrotic proteins and processes in the EAT secretome and EAT from patients with, who will develop (future onset), and without AF. Methods: Atrial EAT was obtainded during thoracoscopic ablation (AF, n = 20), or open-heart surgery (future onset and non-AF, n = 35). ECM gene expression of human atrial fibroblasts exposed to the EAT secretome and the proteomes of EAT secretome and EAT were assessed in patients with and without AF. Myeloperoxidase and neutrophil extracellular traps (NETs) were assessed immunohistochemically in patients with paroxysmal, persistent, future onset, and those who remain free of AF (non-AF). Results: The expression of COL1A1 and FN1 in fibroblasts exposed to secretome from patients with AF was 3.7 and 4.7 times higher than in patients without AF (p < 0.05). Myeloperoxidase was the most increased protein in the EAT secretome and EAT from patients with versus without AF (FC 18.07 and 21.57, p < 0.005), as was the gene-set neutrophil degranulation. Immunohistochemically, myeloperoxidase was highest in persistent (FC 13.3, p < 0.0001) and increased in future onset AF (FC 2.4, p = 0.02) versus non-AF. Myeloperoxidase aggregated subepicardially and around fibrofatty infiltrates. NETs were increased in patients with persistent versus non-AF (p = 0.03). Conclusion: In AF, the EAT secretome induces ECM gene expression in atrial fibroblasts and contains abundant myeloperoxidase. EAT myeloperoxidase was increased prior to AF onset, and both myeloperoxidase and NETs were highest in persistent AF, highlighting the role of EAT neutrophils in the pathophysiology of AF.

Published
2023

5. NOX2 and NOX5 are increased in cardiac microvascular endothelium of deceased COVID-19 patients

Author

Jiang, Zhu, Wu, Linghe, van der Leeden, Britt, van Rossum, Albert C, Niessen, Hans W M, Krijnen, Paul A J, Pathology, ACS - Heart failure & arrhythmias, ACS - Atherosclerosis & ischemic syndromes, Molecular cell biology and Immunology, Cardiology, and AII - Inflammatory diseases

Subjects
NADPH Oxidase 5, Humans, NADPH Oxidases, COVID-19, Heart, Endothelium, Vascular, Reactive Oxygen Species, Cardiology and Cardiovascular Medicine
Abstract

BACKGROUND: Cardiac injury and inflammation are common findings in COVID-19 patients. Autopsy studies have revealed cardiac microvascular endothelial damage and thrombosis in COVID-19 patients, indicative of microvascular dysfunction in which reactive oxygen species (ROS) may play a role. We explored whether the ROS producing proteins NOX2, NOX4 and NOX5 are involved in COVID-19-induced cardio-microvascular endothelial dysfunction.METHODS: Heart tissue were taken from the left (LV) and right (RV) ventricle of COVID-19 patients (n = 15) and the LV of controls (n = 14) at autopsy. The NOX2-, NOX4-, NOX5- and Nitrotyrosine (NT)-positive intramyocardial blood vessels fractions were quantitatively analyzed using immunohistochemistry.RESULTS: The LV NOX2+, NOX5+ and NT+ blood vessels fractions in COVID-19 patients were significantly higher than in controls. The fraction of NOX4+ blood vessels in COVID-19 patients was comparable with controls. In COVID-19 patients, the fractions of NOX2+, NOX5+ and NT+ vessels did not differ significantly between the LV and RV, and correlated positively between LV and RV in case of NOX5 (r = 0.710; p = 0.006). A negative correlation between NOX5 and NOX2 (r = -0.591; p = 0.029) and between NOX5 and disease time (r = -0.576; p = 0.034) was noted in the LV of COVID-19 patients.CONCLUSION: We show the induction of NOX2 and NOX5 in the cardiac microvascular endothelium in COVID-19 patients, which may contribute to the previously observed cardio-microvascular dysfunction in COVID-19 patients. The exact roles of these NOXes in pathogenesis of COVID-19 however remain to be elucidated.

Published
2023

6. IFT74 variants cause skeletal ciliopathy and motile cilia defects in mice and humans

Author

Bakey, Zeineb, primary, Cabrera, Oscar A., additional, Hoefele, Julia, additional, Antony, Dinu, additional, Wu, Kaman, additional, Stuck, Michael W., additional, Micha, Dimitra, additional, Eguether, Thibaut, additional, Smith, Abigail O., additional, van der Wel, Nicole N., additional, Wagner, Matias, additional, Strittmatter, Lara, additional, Beales, Philip L., additional, Jonassen, Julie A., additional, Thiffault, Isabelle, additional, Cadieux-Dion, Maxime, additional, Boyes, Laura, additional, Sharif, Saba, additional, Tüysüz, Beyhan, additional, Dunstheimer, Desiree, additional, Niessen, Hans W. M., additional, Devine, William, additional, Lo, Cecilia W., additional, Mitchison, Hannah M., additional, Schmidts, Miriam, additional, and Pazour, Gregory J., additional

Published
2023
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7. Increased epicardial nerves and decreased intramyocardial PVAT in acute myocardial infarction.

Author

Fiet, Mitchell D., Azouz, Bouchra, Robbers, Lourens F. H. J., Niessen, Hans W. M., and Krijnen, Paul A. J.

Subjects
ATHEROSCLEROTIC plaque, MYOCARDIAL infarction, NERVES, CORONARY artery stenosis, ST elevation myocardial infarction, ORGANIC cation transporters
Abstract

Keywords: cardiovascular disease; coronary artery; myocardial infarction; perivascular nerve fibres; PVAT EN cardiovascular disease coronary artery myocardial infarction perivascular nerve fibres PVAT 1 8 8 10/18/23 20231101 NES 231101 INTRODUCTION Acute myocardial infarction (AMI) primarily results from thrombus formation following plaque rupture in the epicardial coronary arteries (ECA), leading to a partial or complete occlusion of the coronary artery, with subsequent ischemia and infarction of the associated myocardium. As AMI patients died within 6 h after onset of AMI, the PVNF densities were likely increased prior to AMI development. Given that significant atherosclerosis, indicative of endothelial dysfunction and stenosis were present in the ECAs of AMI patients, such increased PVNF activity may possibly have contributed to the onset of AMI. Contrastingly, more PVNF in the AMI group were observed than in control patients, indicating an association between PVNF and AMI. [Extracted from the article]

Published
2023
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10. Elevated monocyte-specific type I interferon signalling correlates positively with cardiac healing in myocardial infarct patients but interferon alpha application deteriorates myocardial healing in rats

Author

ter Horst, Ellis N., Krijnen, Paul A. J., Hakimzadeh, Nazanin, Robbers, Lourens F. H. J., Hirsch, Alexander, Nijveldt, Robin, Lommerse, Ingrid, Fontijn, Ruud D., Meinster, Elisa, Delewi, Ronak, van Royen, Niels, Zijlstra, Felix, van Rossum, Albert C., van der Schoot, C. Ellen, van der Pouw Kraan, Tineke C. T. M., Horrevoets, Anton J., van der Laan, Anja M., Niessen, Hans W. M., and Piek, Jan J.

Published
2019
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12. Systematic study of tissue factor expression in solid tumors

Author

de Bono, Johann S., primary, Harris, Jeffrey R., additional, Burm, Saskia M., additional, Vanderstichele, Adriaan, additional, Houtkamp, Mischa A., additional, Aarass, Saida, additional, Riisnaes, Ruth, additional, Figueiredo, Ines, additional, Nava Rodrigues, Daniel, additional, Christova, Rossitza, additional, Olbrecht, Siel, additional, Niessen, Hans W. M., additional, Ruuls, Sigrid R., additional, Schuurhuis, Danita H., additional, Lammerts van Bueren, Jeroen J., additional, Breij, Esther C. W., additional, and Vergote, Ignace, additional

Published
2022
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17. Clusterin is increased in morphologically normal cardiomyocytes in lymphocytic myocarditis.

Author

Fiet, Mitchell D., Wu, Linghe, Koo, Amy, Woudstra, Linde, Niessen, Hans W. M., and Krijnen, Paul A. J.

Subjects
CLUSTERIN, MYOCARDITIS, COCAINE, COCAINE-induced disorders, ECULIZUMAB, TUKEY'S test
Abstract

We previously observed an increased presence of the stress response protein clusterin in the hearts of acute myocardial infarction patients.[3] Herein, clusterin was not only present in necrotic cardiomyocytes but also in viable morphologically normal cardiomyocytes in the noninfarcted myocardium. Keywords: cardiomyocytes; clusterin; lymphocytic myocarditis; viral myocarditis EN cardiomyocytes clusterin lymphocytic myocarditis viral myocarditis 1 6 6 02/14/23 20230301 NES 230301 INTRODUCTION Myocarditis is an inflammatory disease of the heart that is most commonly caused by a viral infection of the heart. Clusterin+ cardiomyocytes were found scattered across the left ventricle in LM patients and the staining intensity of clusterin varied between cardiomyocytes (Figure 1B). [Extracted from the article]

Published
2023
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18. Systematic study of tissue factor expression in solid tumors.

Author

de Bono, Johann S., Harris, Jeffrey R., Burm, Saskia M., Vanderstichele, Adriaan, Houtkamp, Mischa A., Aarass, Saida, Riisnaes, Ruth, Figueiredo, Ines, Nava Rodrigues, Daniel, Christova, Rossitza, Olbrecht, Siel, Niessen, Hans W. M., Ruuls, Sigrid R., Schuurhuis, Danita H., Lammerts van Bueren, Jeroen J., Breij, Esther C. W., and Vergote, Ignace

Published
2023
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25. Homocysteine-Induced Apoptosis in Endothelial Cells Coincides With Nuclear NOX2 and Peri-nuclear NOX4 Activity

Author

Sipkens, Jessica A., Hahn, Nynke, van den Brand, Carlien S., Meischl, Christof, Cillessen, Saskia A. G. M., Smith, Desirée E. C., Juffermans, Lynda J. M., Musters, René J. P., Roos, Dirk, Jakobs, Cornelis, Blom, Henk J., Smulders, Yvo M., Krijnen, Paul A. J., Stehouwer, Coen D. A., Rauwerda, Jan A., van Hinsbergh, Victor W. M., and Niessen, Hans W. M.

Published
2013
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27. Diaphragm Muscle Fiber Weakness and Ubiquitin-Proteasome Activation in Critically Ill Patients

Author

Hooijman, Pleuni E., Beishuizen, Albertus, Witt, Christian C., de Waard, Monique C., Girbes, Armand R. J., Spoelstra-de Man, Angelique M. E., Niessen, Hans W. M., Manders, Emmy, van Hees, Hieronymus W. H., van den Brom, Charissa E., Silderhuis, Vera, Lawlor, Michael W., Labeit, Siegfried, Stienen, Ger J. M., Hartemink, Koen J., Paul, Marinus A., Heunks, Leo M. A., and Ottenheijm, Coen A. C.

Published
2015
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28. Myocardial infarction accelerates atherosclerosis

Author

Dutta, Partha, Courties, Gabriel, Wei, Ying, Leuschner, Florian, Gorbatov, Rostic, Robbins, Clinton S., Iwamoto, Yoshiko, Thompson, Brian, Carlson, Alicia L., Heidt, Timo, Majmudar, Maulik D., Lasitschka, Felix, Etzrodt, Martin, Waterman, Peter, Waring, Michael T., Chicoine, Adam T., van der Laan, Anja M., Niessen, Hans W. M., Piek, Jan J., Rubin, Barry B., Butany, Jagdish, Stone, James R., Katus, Hugo A., Murphy, Sabina A., Morrow, David A., Sabatine, Marc S., Vinegoni, Claudio, Moskowitz, Michael A., Pittet, Mikael J., Libby, Peter, Lin, Charles P., Swirski, Filip K., Weissleder, Ralph, and Nahrendorf, Matthias

Published
2012
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30. Viral presence and immunopathology in patients with lethal COVID-19: a prospective autopsy cohort study: a prospective autopsy cohort study

Author

Schurink, Bernadette, Roos, Eva, Radonic, Teodora, Barbe, Ellis, Bouman, Catherine S. C., de Boer, Hans H., de Bree, Godelieve J., Bulle, Esther B., Aronica, Eleonora M., Florquin, Sandrine, Fronczek, Judith, Heunks, Leo M. A., de Jong, Menno D., Guo, Lihui, du Long, Romy, Lutter, Rene, Molenaar, Pam C. G., Neefjes-Borst, E. Andra, Niessen, Hans W. M., van Noesel, Carel J. M., Roelofs, Joris J. T. H., Snijder, Eric J., Soer, Eline C., Verheij, Joanne, Vlaar, Alexander P. J., Vos, Wim, van der Wel, Nicole N., van der Wal, Allard C., van der Valk, Paul, Bugiani, Marianna, Intensive Care Medicine, Infectious diseases, AII - Infectious diseases, APH - Aging & Later Life, APH - Global Health, Graduate School, Pathology, APH - Mental Health, ANS - Cellular & Molecular Mechanisms, Pulmonology, ACS - Diabetes & metabolism, ACS - Microcirculation, Medical Biology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, ACS - Heart failure & arrhythmias, and ACS - Pulmonary hypertension & thrombosis

Abstract

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) targets multiple organs and causes severe coagulopathy. Histopathological organ changes might not only be attributable to a direct virus-induced effect, but also the immune response. The aims of this study were to assess the duration of viral presence, identify the extent of inflammatory response, and investigate the underlying cause of coagulopathy. Methods: This prospective autopsy cohort study was done at Amsterdam University Medical Centers (UMC), the Netherlands. With informed consent from relatives, full body autopsy was done on 21 patients with COVID-19 for whom autopsy was requested between March 9 and May 18, 2020. In addition to histopathological evaluation of organ damage, the presence of SARS-CoV-2 nucleocapsid protein and the composition of the immune infiltrate and thrombi were assessed, and all were linked to disease course. Findings: Our cohort (n=21) included 16 (76%) men, and median age was 68 years (range 41–78). Median disease course (time from onset of symptoms to death) was 22 days (range 5–44 days). In 11 patients tested for SARS-CoV-2 tropism, SARS-CoV-2 infected cells were present in multiple organs, most abundantly in the lungs, but presence in the lungs became sporadic with increased disease course. Other SARS-CoV-2-positive organs included the upper respiratory tract, heart, kidneys, and gastrointestinal tract. In histological analyses of organs (sampled from nine to 21 patients per organ), an extensive inflammatory response was present in the lungs, heart, liver, kidneys, and brain. In the brain, extensive inflammation was seen in the olfactory bulbs and medulla oblongata. Thrombi and neutrophilic plugs were present in the lungs, heart, kidneys, liver, spleen, and brain and were most frequently observed late in the disease course (15 patients with thrombi, median disease course 22 days [5–44]; ten patients with neutrophilic plugs, 21 days [5–44]). Neutrophilic plugs were observed in two forms: solely composed of neutrophils with neutrophil extracellular traps (NETs), or as aggregates of NETs and platelets. Interpretation: In patients with lethal COVID-19, an extensive systemic inflammatory response was present, with a continued presence of neutrophils and NETs. However, SARS-CoV-2-infected cells were only sporadically present at late stages of COVID-19. This suggests a maladaptive immune response and substantiates the evidence for immunomodulation as a target in the treatment of severe COVID-19. Funding: Amsterdam UMC Corona Research Fund.

Published
2020

36. The histopathological spectrum of myocardial inflammation in relation to circumstance of death: a retrospective cohort study in clinical and forensic autopsies.

Author

du Long, Romy, Fronczek, Judith, Niessen, Hans W. M., van der Wal, Allard C., and de Boer, Hans H.

Subjects
AUTOPSY, HISTOPATHOLOGY, CAUSES of death, COHORT analysis, INFLAMMATION, RETROSPECTIVE studies
Abstract

Interpreting a myocardial inflammation as causal, contributory or as of no significance at all in the cause of death can be challenging, especially in cases where other pathologic and/or medico-legal findings are also present. To further evaluate the significance of myocardial inflammation as a cause of death we performed a retrospective cohort study of forensic and clinical autopsy cases. We revised the spectrum of histological inflammatory parameters in the myocardium of 79 adult autopsy cases and related these to the reported cause of death. Myocardial slides were reviewed for the distribution and intensity of inflammatory cell infiltrations, the predominant inflammatory cell type, and the presence of inflammation-associated myocyte injury, fibrosis, edema and hemorrhage. Next, the cases were divided over three groups, based on the reported cause of death. Group 1 (n = 27) consisted of all individuals with an obvious unnatural cause of death. Group 2 (n = 29) included all individuals in which myocarditis was interpreted to be one out of more possible causes of death. Group 3 (n = 23) consisted of all individuals in which myocarditis was reported to be the only significant finding at autopsy, and no other cause of death was found. Systematic application of our histological parameters showed that only a diffuse increase of inflammatory cells could discriminate between an incidental presence of inflammation (Group 1) or a potentially significant one (Groups 2 and 3). No other histological parameter showed significant differences between the groups. Our results suggest that generally used histological parameters are often insufficient to differentiate an incidental myocarditis from a (potentially) significant one. [ABSTRACT FROM AUTHOR]

Published
2022
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38. Homocysteine affects cardiomyocyte viability: concentration-dependent effects on reversible flip-flop, apoptosis and necrosis

Author

Sipkens, Jessica A., Krijnen, Paul A. J., Meischl, Christof, Cillessen, Saskia A. G. M., Smulders, Yvo M., Smith, Desirée E. C., Giroth, Cindy P. E., Spreeuwenberg, Marieke D., Musters, René J. P., Muller, Alice, Jakobs, Cornelis, Roos, Dirk, Stehouwer, Coen D. A., Rauwerda, Jan A., van Hinsbergh, Victor W. M., and Niessen, Hans W. M.

Published
2007
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45. Apoptosis in diabetes

Author

Krijnen, Paul A. J., Simsek, Suat, and Niessen, Hans W. M.

Published
2009

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