Bente Halvorsen1, Martine Z Espeland2, Geir Øystein Andersen3, Arne Yndestad4, Ellen Lund Sagen2, Azita Rashidi5, Eva C Knudsen6, Mona Skjelland7, Karolina R Skagen7, Kirsten Krohg-Sørensen8, Sverre Holm5, Vibeke Ritschel6, Kirsten B Holven9, Erik A L Biessen10, Pål Aukrust11, Tuva B Dahl12. 1. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway. 2. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. 3. Department of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway; Center for Heart Failure, University of Oslo, Oslo, Norway. 4. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Center for Heart Failure, University of Oslo, Oslo, Norway. 5. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway. 6. Department of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway; Center for Clinical Heart Research, Oslo University Hospital Ullevål, Oslo, Norway. 7. Department of Neurology, Oslo University Hospital Rikshospitalet, Oslo, Norway. 8. Department of Thoracic and Cardiovascular Surgery Oslo University Hospital Rikshospitalet, Oslo, Norway. 9. Department of Nutrition, Institute for Basic Medical Sciences, University of Oslo, Norway. 10. Experimental Vascular Pathology Group, Department of Pathology, CARIM, Maastricht University Medical Center, Maastricht, The Netherlands. 11. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Disease, Oslo University Hospital Rikshospitalet, Oslo, Norway. 12. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway. Electronic address: tuvad@rr-research.no.
Abstract
AIM: The aim of the present study were to elucidate the role of NAMPT in atherosclerosis, by examine NAMPT expression in peripheral blood mononuclear cells (PBMC) in patients with coronary artery disease (CAD) and healthy controls and by examining the regulation and effect of NAMPT on macrophage polarization, hypothesizing that it could influence the polarization to inflammatory and resolving macrophages. METHOD AND RESULTS: We analyzed RNA levels of NAMPT in PBMC from CAD and healthy controls and found NAMPT to be increased in PBMC from patients with acute coronary syndrome (n = 39) compared to healthy controls (n = 20) and patients with stable CAD (n = 22). Within the PBMC NAMPT was correlated to several inflammatory cytokines and the antioxidant enzyme superoxide dismutase 2. In vitro cell experiments revealed that NAMPT is increased both intracellular and extracellular in inflammatory M1 macrophages compared to in anti-inflammatory M2 macrophages. In addition, inhibiting NAMPT enzymatic activity inhibited M1 polarization in macrophages. CONCLUSION: Based on our in vivo and in vitro findings we suggest that NAMPT could contribute to systemic and plaque inflammation in atherosclerotic disorders at least partly through effect on macrophages.
AIM: The aim of the present study were to elucidate the role of NAMPT in atherosclerosis, by examine NAMPT expression in peripheral blood mononuclear cells (PBMC) in patients with coronary artery disease (CAD) and healthy controls and by examining the regulation and effect of NAMPT on macrophage polarization, hypothesizing that it could influence the polarization to inflammatory and resolving macrophages. METHOD AND RESULTS: We analyzed RNA levels of NAMPT in PBMC from CAD and healthy controls and found NAMPT to be increased in PBMC from patients with acute coronary syndrome (n = 39) compared to healthy controls (n = 20) and patients with stable CAD (n = 22). Within the PBMC NAMPT was correlated to several inflammatory cytokines and the antioxidant enzyme superoxide dismutase 2. In vitro cell experiments revealed that NAMPT is increased both intracellular and extracellular in inflammatory M1 macrophages compared to in anti-inflammatory M2 macrophages. In addition, inhibiting NAMPT enzymatic activity inhibited M1 polarization in macrophages. CONCLUSION: Based on our in vivo and in vitro findings we suggest that NAMPT could contribute to systemic and plaque inflammation in atherosclerotic disorders at least partly through effect on macrophages.
Authors: Na Xie; Lu Zhang; Wei Gao; Canhua Huang; Peter Ernst Huber; Xiaobo Zhou; Changlong Li; Guobo Shen; Bingwen Zou Journal: Signal Transduct Target Ther Date: 2020-10-07
Authors: Rania El Fekih; James Hurley; Vasisht Tadigotla; Areej Alghamdi; Anand Srivastava; Christine Coticchia; John Choi; Hazim Allos; Karim Yatim; Juliano Alhaddad; Siawosh Eskandari; Philip Chu; Albana B Mihali; Isadora T Lape; Mauricio P Lima Filho; Bruno T Aoyama; Anil Chandraker; Kassem Safa; James F Markmann; Leonardo V Riella; Richard N Formica; Johan Skog; Jamil R Azzi Journal: J Am Soc Nephrol Date: 2021-03-03 Impact factor: 10.121
Authors: Hilde L Orrem; Per H Nilsson; Søren E Pischke; Ola Kleveland; Arne Yndestad; Karin Ekholt; Jan K Damås; Terje Espevik; Bjørn Bendz; Bente Halvorsen; Ida Gregersen; Rune Wiseth; Geir Ø Andersen; Thor Ueland; Lars Gullestad; Pål Aukrust; Andreas Barratt-Due; Tom E Mollnes Journal: Front Immunol Date: 2018-09-12 Impact factor: 7.561