Group index

Christensen Research group

Geir Christensen 5x7
Group leader: professor Geir Christensen

Cellular and molecular biology of myocardial hypertrophy and heart failure

Geir Christensen is leader of Center for Heart Failure Research and Norwegian PhD School of Heart Research (NORHEART). The work in his group aims to develop novel therapeutic approaches and better diagnostic tools for heart failure through new knowledge about molecular mechanisms involved.

In particular, the group is studying the concept that cardiac proteoglycans are active and central signal mediators of myocardial remodeling. Proteoglycans are highly glycosylated proteins localized to the cell membranes and the extracellular matrix (ECM). By examining the unique properties of transmembrane proteoglycans we have discovered that the proteoglycan syndecan-4 is a mechanical stress-sensor in cardiomyocytes and cardiac fibroblasts and involved in signalling causing heart failure. One important ECM-localized molecule is lumican and we have shown that it regulates cardiac remodelling and heart failure. Currently we are testing promising drugs to treat heart failure by targeting mechanisms identified by our group. The ultimate goal of all medical research is to improve the well-being and prognosis of patients. Thus, we have established a group consisting of scientists from IEMR that collaborate closely with Department of Thoracic Surgery (Professor Theis Tønnessen) and Department of Cardiology at Oslo University Hospital (Professor Lars Gullestad), and top-of-the-range international scientists from Harvard, Johns Hopkins, among others, who are world leading in their field.

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Center for Heart Failure Research
Norwegian PhD School of Heart Research (NORHEART)

Figure. Pressure overload induces remodeling of the myocardium that ultimately results in heart failure. We propose that proteoglycans located to the ECM (ECM-localized) and in the plasma membrane (membrane-bound) of cardiac fibroblasts actively regulate myocardial fibrosis by inducing myofibroblast differentiation and ECM production in response to mechanical stress.

Sjaastad Research group

Ivar Sjaastad
Group leader: professor Ivar Sjaastad

Disease mechanisms of heart failure

Ivar Sjaastad is a cardiologist and leader of the KG Jebsen Center for Cardiac Research and a core facility for preclinical MRI. His research is both clinical and basic science. He has a translational approach, and the ultimate goal is to develop new therapeutic strategies improving cardiac contraction and relaxation in heart failure.

We aim to unravel the disease mechanisms underlying heart failure, with special emphasis on how mechanical stress translates into pathological cardiac relaxation. We develop and refine beyond state of the art high resolution MR imaging techniques, including phase contrast, diffusion techniques and T1 mapping, to in detail examine and understand

the structure-function relationship in the remodeled heart. Advanced imaging techniques are used to assess the impact of systemic inflammation on cardiac function, including cardiac arrhythmias. Cardiac arrhythmias are important causes of mortality in

heart failure, and the intracellular signaling pathways underlying such arrhythmias is largely unknown. We thus focus on cardiomyocyte signaling pathways, both physiological and pathophysiological aspects. Special emphasis is put on the intracellular signaling molecules involved in betaadrenergic signaling, which both can regulate cardiac rhythm and relaxation. In this context, the regulatory role of phosphodiesterases (PDEs) is explored. Their role in cardiac dysfunction is investigated both at the cellular and organ level, and a potential therapeutic effect is scrutinized.

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Figure. The cardiac cells respond to mechanical stress, potentially resulting in cardiac dysfunction and heart failure.

Louch Research group

Bill Louch  5x7 valgt
Group leader: professor William E. Louch

Cardiomyocyte function in health and disease

Bill Louch is a Professor of Medicine and head of the Core Facility for Advanced Light Microscopy. He currently holds a Consolidator Grant from the European Research Council which was initiated in 2015. His research team aims to develop new therapies which target cardiac muscle cells for the benefit of the cardiac patient.

My group’s research is focused on the structure and function cardiac muscle cells. Cardiac function is tightly controlled by the contraction and relaxation of these cells; processes which are in turn reliant on carefully controlled calcium homeostasis. Indeed, cardiac dysfunction during diseases such as heart failure and atrial fibrillation can often be traced to abnormal cellular calcium handling.

Our research is aimed at understanding these abnormalities, with focus on the structures and proteins that control calcium cycling. How are these structures and proteins put together during development, and what causes them to disassemble during disease? What is the consequence of such alterations? To examine these questions, we combine molecular biology and electrophysiology techniques with advanced 3D imaging (super-resolution, confocal, and electron microscopy).
Ultimately, we strive to mechanistically link subcellular structure and calcium handling to whole-heart function, and to reverse dysfunction during disease.

Figure. Key players controlling cardiomyocyte structure and function.

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Cataliotti Research group

Group leader: Professor Alessandro Cataliotti

The endocrine function of the heart

Alessandro Cataliotti is a Professor of Medicine and has joined the University of Oslo at the IEMR three years ago after conducting extensive research in the field of cardiovascular disease in the USA at the prestigious location of the Mayo Clinic Foundation. He has conducted several preclinical and clinical studies to evaluate the effects of cardiac hormones in the setting of cardiovascular and renal dysfunction and has received numerous international scientific awards and nominations in recognition of his work.

Starting from the understanding of the existence of an impaired endocrine function of the heart that underlies several cardiovascular and renal diseases in humans, our group investigates the hormonal function of the heart in both physiological and pathophysiological conditions. The main focus of our group is to study the role of hormones produced by the heart during the early stages of human cardiovascular and renal dysfunction, such as hypertension, stage A-B heart failure, ischemic cardiomyopathy, and mild to moderate renal impairment. Our group has a highly translational approach, performing both clinical studies, and preclinical research using innovative delivery approaches, as well as new therapeutic agents such as alternative forms of natriuretic peptides. Our group is also committed to the discovery of novel small molecules that can enhance the activity of the cardiac peptides, and to further elucidate the mechanisms of actions of molecules known to interfere with the activity of several cardiac hormones.

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Figure. Simplified examples of the endocrine function of the heart in humans limited to two well-known cardiac hormones, the atrial natriuretic peptide (ANP) and the B-type natriuretic peptide (BNP), through the activation of guanylyl cyclase A (GC-A) stress (Kuhn et al., Physiol Rev 2016).

Carlson Research group

Cathrine Carlson 5x7
Group leader and PI: Dr. Cathrine Rein Carlson

Molecular mechanisms of signal transduction in heart

Dr. Cathrine Rein Carlson is principal investigator and group leader at the Institute for Experimental Medical Research.
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My research group focuses on defining molecular mechanisms and the intracellular communication networks that promote specificity in signal transduction in the heart. In particular, we work on various ion channels and exchangers, proteoglycans, kinases and phosphatases and changes in these protein complexes during development of heart failure (figure 1 below).

In our projects we use a range of molecular biology techniques combined with peptide technology. In particular, we identify various protein interactomes and protein-protein interactions down to the amino acid level to further develop high affinity peptide disruptors to block harmful signaling events (pro-drugs, illustrated in figure 2 below). The peptide disruptors are introduced into various cell cultures and primary cardiac cells by adding a cell-permeable tag or into animals by adeno-associated virus technology or by making transgenic animals.

We have several top-of-the-range national and international collaborators.

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Figure 1: (Finsen et al., Plos One, 6(12):e28302, 2011)

Figure 2: (Wanichawan et al.,Biochem J, 473(15):2413-23, 2016)

Lunde Research group

Ida Gjervold Lunde
Group leader and PI: Dr. Ida Gjervold Lunde

Experimental Genetic Cardiology

Dr. Ida Gjervold Lunde is principal investigator and group leader at the Institute for Experimental Medical Research.

Click for Ida Gjervold Lunde profile page.

Millions of patients worldwide suffer from heart failure. Heart failure is a chronic, deadly and costly syndrome, and we currently have no cure. Thus, research into its underlying molecular basis is necessary in order to understand the disease mechanisms, and thereby, design effective medical therapy to improve patient outcome.

Heart failure is often familial, suggesting a genetic cause.

We are a basic science cardiology group working on experimental models of heart failure, with particular focus on genetic heart failure. We are based at IEMR at OUH and UoO, and have extensive national and international research collaboration. We combine a range of molecular biology techniques and analyses, and aim at unravelling pathophysiological processes and mechanisms underlying heart failure.

In particular, we are interested in understanding the role of proteoglycans and titin in the heart.

Our experimental models and samples include heart biopsies from patients, mouse models with overexpression or knock-out of proteins, mouse models with human disease-causing mutations (e.g. familial HCM and DCM),

heart tissue from mice and rats, and cultures of cardiac cells such as fibroblasts and cardiomyocytes.
Close collaborations with the Christensen, Tønnessen and Carlson Research Groups at IEMR.

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For publications, please see PubMed

Stokke Research group

Translational arrhythmology and electrophysiology

Mathis Korseberg Stokke is Associate Professor I at UiO and consultant at the Arrhythmia Unit, Department of Cardiology, Oslo University Hospital Rikshospitalet. He is Deputy Director of NORHEART – The Norwegian PhD School of Heart Research. His research group aims to understand processes that lead to cardiac disease due to pathological electrophysiology, especially arrhythmias.

We want to be able to predict and prevent triggers of arrhythmic events, and to provide a basis for the use of exercise for electrophysiological remodeling in a safe manner. We combine clinical observations and interventions with rodent models of heart failure, CPVT, HCM and ischemia-reperfusion. We especially focus on proteins involved in Ca2+ handling, such as RyR2, SERCA2 and CaMKII. We use molecular biology, cellular electrophysiology, Langendorff-perfused hearts, and in vivo characterization by echocardiography, MRI and telemetric ECG recording, as well as exercise training by treadmills and resistance-controlled running wheels.

The personnel in our group have different academic backgrounds and specific know-how, from nanotechnology and molecular biology to clinical training in cardiology. We also collaborate closely with other research groups with expertise on basic research methods, clinical electrophysiology, cardiac imaging and cardiogenetics. This give us the opportunity to understand biological processes involved in pathological electrophysiology on a molecular, cellular, organ and organism level.

A Illustration of cardiac electro-mechanical coupling.

B Normal and arrhythmogenic Ca2+ release events.

C Bidirectional VT from CPVT mouse.

D Mouse echocardiography.

E Mouse cardiac MRI.

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