Siril Skaret Bakke
Siril Skaret Bakke
Researcher at CEMIR/Advisor at Klinforsk
MH Faculty Administration Faculty of Medicine and Health Sciences Department of Clinical and Molecular MedicineBackground and activities
I am a civil engineer in biotechnology and a PhD in pharmacology. Previously, I have worked in several laboratories both nationally and internationally within different disciplines. Through my PhD I became a specialist in lipid metabolism associated with type 2 diabetes and obesity in muscle cells. I also have experience with different live cell imaging techniques and teaching, as well as analysis with big gene expression data sets.
I work at Centre of Molecular Inflammation Research (CEMIR) at NTNU. As a post doc I was working on revealing the mechanisms behind inflammation and complement system activation in regards to cholesterol crystal accumulation in atherosclerotic plaques and to find new novel treatments against atherosclerosis.15 september 2014 - 1st of june I was in the lab of Prof Eicke Latz, Institute of Innate Immunity, University of Bonn, Germany. Now I work as a researcher studying TLR4 mediated signalling in relation to human diseases.
In addition, I work as a consultant for the clinical research unit Central Norway (Klinforsk). I work as a consultant in data management for clinical studies and am a super user for eFORSK.
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
Journal publications
- (2020) Cholesterol crystals use complement to increase NLRP3 signaling pathways in coronary and carotid atherosclerosis. EBioMedicine. vol. 60:102985.
- (2019) Serum Omega-6 Fatty Acids and Immunology-Related Gene Expression in Peripheral Blood Mononuclear Cells: A Cross-Sectional Analysis in Healthy Children. Molecular Nutrition & Food Research. vol. 63 (7).
- (2019) Genetic Variation/Evolution and Differential Host Responses Resulting from In-Patient Adaptation of Mycobacterium avium. Infection and Immunity. vol. 87 (4).
- (2019) Increased glycolysis and higher lactate production in hyperglycemic myotubes. Cells. vol. 8 (9).
- (2019) Profiling of immune-related gene expression in children with familial hypercholesterolaemia. Journal of Internal Medicine.
- (2019) Alpha-cyclodextrin inhibits cholesterol crystal-induced complement-mediated inflammation: A potential new compound for treatment of atherosclerosis. Atherosclerosis. vol. 283.
- (2018) Increased triacylglycerol - Fatty acid substrate cycling in human skeletal muscle cells exposed to eicosapentaenoic acid. PLOS ONE. vol. 13:e0208048 (11).
- (2017) Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation. Journal of Immunology. vol. 199 (8).
- (2017) Loss of perilipin 2 in cultured myotubes enhances lipolysis and redirects the metabolic energy balance from glucose oxidation towards fatty acid oxidation. Journal of Lipid Research. vol. 58 (11).
- (2016) Cholesterol crystals activate the lectin complement pathway via ficolin-2 and mannose-binding lectin: Implications for the progression of atherosclerosis. Journal of Immunology. vol. 196 (12).
- (2016) Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming. Science Translational Medicine. vol. 8 (333).
- (2015) Myotubes from Severely Obese Type 2 Diabetic Subjects Accumulate Less Lipids and Show Higher Lipolytic Rate than Myotubes from Severely Obese Non-Diabetic Subjects. PLOS ONE. vol. 10 (3).
- (2015) Myotubes from lean and severely obese subjects with and without type 2 diabetes respond differently to an in vitro model of exercise. American Journal of Physiology - Cell Physiology. vol. 308 (7).
- (2015) Primary defects in lipolysis and insulin action in skeletal muscle cells from type 2 diabetic individuals. Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. vol. 1851 (9).
- (2015) Reconstituted high-density lipoprotein attenuates cholesterol crystal-induced inflammatory responses by reducing complement activation. Journal of Immunology. vol. 195 (1).
- (2014) PPARδ activation in human myotubes increases mitochondrial fatty acid oxidative capacity and reduces glucose utilization by a switch in substrate preference. Archives of Physiology and Biochemistry. vol. 120 (1).
- (2014) Cholesterol crystals induce complement-dependent inflammasome activation and cytokine release. Journal of Immunology. vol. 192 (6).
- (2013) Are cultured human myotubes far from home?. Cell and Tissue Research. vol. 354 (3).
- (2013) Remodelling of oxidative energy metabolism by galactose improves glucose handling and metabolic switching in human skeletal muscle cells. PLOS ONE. vol. 8 (4).
- (2012) Palmitic acid follows a different metabolic pathway than oleic acid in human skeletal muscle cells; lower lipolysis rate despite an increased level of adipose triglyceride lipase. Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. vol. 1821 (10).