Spring Selection 2018

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closes 7 Jan 2018

Research Groups

Portrait Henning Morawietz

Henning Morawietz

Endothelium and cardiovascular diseases

Previous and Current Research

Cardiovascular diseases are the major cause of mortality in the industrial countries. Arteriosclerosis is considered to play a key role in this process, because the progression of this disease increases the risk of hypertension, coronary heart disease, heart attack and stroke. The endothelial cells form the inner layer of the blood vessels and play an important in the development and progression of arteriosclerosis.

Local differences in hemodynamic forces acting by the flowing blood on the cells of the vessel wall have been postulated as a putative mechanism for the localization of arteriosclerotic plaques. One major focus of our research is therefore the identification of molecular changes in response to different hemodynamic forces in human endothelial cells. A second research focus is the investigation of putative proarteriosclerotic mechanisms like increased NAD(P)H oxidase-dependent oxidative stress or augmented uptake of oxidized low-density lipoprotein in endothelial cells. We are interested in the mechanisms of the arteriovenous differentiation of endothelial cells and the formation of new blood vessels. Additional directions of the research are the adrenal gland with special focus on aldosterone, retinal diseases and the impact of risk factors like obesity and diabetes on cardiovascular diseases.

We extend our in vitro studies in experimental and clinical studies in vivo and analyze the putative antiarteriosclerotic potential of pharmacological intervention in the renin-angiotensin-aldosterone system or lipid-lowering drugs.

Henning Morawietz research: figure 1
Fig.1: Occlusion of femoral artery
Henning Morawietz research: figure 2
Fig.2: Development of vascular networks from endothelial cells
Future Projects and Goals

Endothelial cells play a major role in the development and differentiation of the vascular system. The development of a functional vascular system is also a crucial step in survival of regenerating tissue. Risk factors like oxidative stress and low-density lipoproteins can accelerate endothelial dysfunction and arteriosclerosis. In further studies, we will try to understand the molecular mechanisms underlying these processes and develop therapeutic strategies in the treatment of cardiovascular diseases. Using techniques of molecular and cell biology, transgenic models and clinical studies we will try to answer the following questions:

  1. How do risk factors like obesity and diabetes potentiate cardiovascular diseases?
  2. Is the increased formation of reactive oxygen species and oxidized lipoproteins involved in these processes?
  3. How differentiate endothelial cells into an arterial or venous phenotype?
  4. What are the molecular mechanisms of the formation of new blood vessels?
Methodological and Technical Expertise
  • Primary cultures of human endothelial cells
  • Application of biomechanical forces (shear stress, cyclic strain) on cells
  • Promoter deletion studies and transcription factors
  • Experimental models of endothelial dysfunction, obesity and diabetes
  • Clinical studies
Selected Publications

H. Langbein, C. Brunssen, A. Hofmann, P. Cimalla, M. Brux, S. R. Bornstein, A. Deussen, E. Koch, H. Morawietz
NADPH oxidase 4 protects against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice.
Eur. Heart J., 37(22):1753–1761. doi: 10.1093/eurheartj/ehv564 (2016)

S. Korten, C. Brunssen, D. M. Poitz, S. Grossklaus, M. Brux, H. J. Schnittler, R. H. Strasser, S. R. Bornstein, H. Morawietz, W. Goettsch
Impact of Hey2 and COUP-TFII on genes involved in arteriovenous differentiation in primary human arterial and venous endothelial cells.
Basic Res. Cardiol., 108(4):362. doi: 10.1007/s00395-013-0362-0 (2013)

U. Schubert, J. Schmid, S. Lehmann, X. Y. Zhang, H. Morawietz, N. L. Block, W. Kanczkowski, A. V. Schally, S. R. Bornstein, B. Ludwig
Transplantation of pancreatic islets to adrenal gland is promoted by agonists of growth hormone releasing hormone.
Proc. Natl. Acad. Sci. U. S. A., 110, 2288-2293 (2013)

C. Goettsch, W. Goettsch, M. Brux, C. Haschke, C. Brunssen, G. Muller, S. R. Bornstein, N. Duerrschmidt, A. H. Wagner, H. Morawietz
Arterial flow reduces oxidative stress via an antioxidant response element and Oct-1 binding site within the NADPH oxidase 4 promoter in endothelial cells.
Basic. Res. Cardiol., 106, 551-561 (2011)

T. Kampfrath, A. Maiseyeu, Z. Ying, Z. Shah, J. A. Deiuliis, X. Xu, N. Kherada, R. D. Brook, K. M. Reddy, N. P. Padture, S. Parthasarathy, L. C. Chen, S. Moffatt-Bruce, Q. Sun, H. Morawietz, S. Rajagopalan
Chronic fine particulate matter exposure induces systemic vascular dysfunction via NADPH oxidase and TLR4 pathways.
Circ. Res., 108, 716-726 (2011)

CV

since 2015
Chairman Strategy Committee European Society for Microcirculation

since 2014
Secretary General of Society of Microcirculation and Vascular Biology

2012–2013
President of the Society of Microcirculation and Vascular Biology

since 2003
Full Professor and Head of Dept. of Vascular Endothelium and Microcirculation, Medical Clinic and Policlinic III, TU Dresden

2002–2003
Assistant Professor, Institute of Pathophysiology, University of Halle, Germany

1996–2002
Group Leader, Institute of Pathophysiology, University of Halle, Germany

1995–1996
Postdoctoral Fellow, Cardiovascular Research Institute, University of California, San Francisco, California

1994–1995
Group Leader, Institute of Pathophysiology, University of Halle, Germany

1990–1994
Postdoctoral fellow, Institute of Genetics, University of Halle, Germany, Studies at Universities of Cologne (1991) and Geneva (1993)

1990
PhD, University of Halle, Germany

Contact

Medical Theoretical Center (MTZ)
Technische Universität Dresden
Fiedlerstraße 42
01307 Dresden

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