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Über uns

AG Preissner 2018

Our main areas of research: 


Cellular and molecular communications in the vascular system in relation to inflammation

  • The role of matrix proteins, adhesion receptors and protease systems in mechanisms of angiogenesis, atherogenesis and vascular remodeling
  • New adhesion receptors for recruitment and transmigration/invasion of leukocytes in inflammation
  • Mechanism of tumor-necrosis-factor shedding
  • Pathological mechanisms of late complications of diabetes, role of advanced glycation endproducts

 

Mechanisms in innate immunity and body defense with particular emphasis on haemostasis and blood coagulation

  • New intravascular and extravascular initiation mechanisms of blood coagulation
  • Extracellular RNA and NET between defense and disease: contribution in thrombosis, edema, angiogenesis, arteriogenesis and atherosclerosis
  • New intervention strategies in vascular diseases using RNase and DNase
  • Cellular haemostasis and protease receptor-mediated reactions


 

Bacterial invasion and anti-adhesive strategies for anti-microbial therapies

  • Wound healing mechanisms and bacterial infection in vertebrates and insects
  • Bacterial adhesion, invasion and evasion strategies with emphasis on Eap

 

Research Areas of the Preissner Group:

 

The scientific interests and active research of the group are concerned with the contribution of innate immunity processes in host-pathogen interactions, inflammation, wound healing and thrombosis, particularly dedicated to cardiovascular and pulmonary diseases. In this context, the as yet unrecognized role of self-extracellular nucleic acids as alarm signals in disease is a major part of our work, documented by many recent publications, particularly achieved by multiple collaborations with different laboratories worldwide.

 

A major part of our current work concentrates on the role of “danger-associated molecular patterns” (DAMPs) such as endogenous extracellular nucleic acids as alarm signals in situations of microbe-host interactions or in diseases of the vascular and cardiopulmonary system. To this end, our group has made seminal discoveries to show that self-extracellular RNA serves as a potent cofactor in thrombosis, tissue edema, cardiac ischemia-reperfusion injury or tumor progression and that RNase1 administration is successful as novel therapeutic intervention in such pathological situations. Likewise, together with cooperation partners in Munich (Steffen Massberg and Bernd Engelmann), extracellular DNA/histone complexes (released from neutrophils as bacteria-killing “neutrophil extracellular traps”, NETs) have been shown to be principal intravascular initiators of arterial as well as venous thrombosis. Together, these novel concepst have had a major impact on our mechanistic understanding of cardiovascular and inflammatory diseases as well as for the use of potentially novel drugs such as RNase1 or DNase.

 

Previously, our work was concerned with new regulatory mechanisms of blood coagulation and thrombosis at the vessel wall and particularly with the diverse properties of vitronectin, a multifunctional adhesive as regulatory factor in vascular biology. Here, several discoveries, concerned with the scaffolding functions of vitronectin as matricellular protein and its receptors (integrins and non-integrins such as the urokinase receptor), were made, particularly related to inflammation, angiogenesis, and the regulation of other vascular processes.

 

We further described new adhesion receptors (such as JAM-3 or RAGE) in the context of cell-to-cell communication in inflammatory reactions as being responsible for seminal reactions of the leukocyte recruitment process in innate immunity. Our research on a specific adherence protein of Staphylococcus aureus, designated “Extracellular adherence protein” (Eap), which presents strong anti-inflammatory and anti-angiogenic functions, has gained insights into bacteria-protective/evasion properties of this factor. Moreover, Eap has successfully been used as a novel anti-inflammatory approach in diverse animal models for therapeutic intervention in wound healing, multiple sclerosis, psoriasis or tumor metastasis. 

  

Previous and Current Research Activities of the Preissner Group:

 

1983-1988

Regulation of thrombin function at the vascular endothelium, influence of thrombomodulin, serpins and proteoglycans

1985-1999

Structure-function relationships of vitronectin and its receptors, humoral and cellular activities of the matricellular protein

since 1997

Bacteria-host interactions, bacterial adhesion and evasion strategies in infection

1988-1998

Plasminogen activator inhibitor-1 (PAI-1) and its interactions with cells and proteins, role of PAI-1 in cell motility and cell functions

1996-2006

Functions of urokinase receptor as coordinator of cell adhesion and pericellular proteolysis, regulation of ß2-integrin-dependent leukocyte functions

1996-2004

Mechanisms of pathological angiogenesis, diabetic retinopathy (coop Diabetology)

1998-2004

Mechanisms of high-molecular-weight-kininogen as anti-adhesive and anti-inflammatory protein

2001-2011

Structure and function of Factor VII-activating protease (FSAP)

since 2002

Anti-inflammatory and anti-angiogenic mechanisms of “Extracellular adherence protein” (Eap) from Staphylococcus aureus (coop Medical Microbiology)

2002-2006

Discovery and functions of new cell adhesion receptors (JAM-3, RAGE), role in inflammation and thrombosis (coop Transfusion Medicine)

2003-2010

New RNA-binding autoantigens in neurological disorders (coop Neurology)

2004-2010

Vascular stem cells and mechanisms of placenta formation (coop Gynecology)

since 2002

New induction processes in haemostasis and blood coagulation, mechanisms of "Intra-vascular Tissue Factor Pathway"

since 2002

Extracellular RNA as endogenous alarm signal in body defense and cardio-vascular diseases

since 2005

Inflammatory and degenerative mechanisms in lung diseases, cellular activities of intrinsic coagulation in lung fibrosis (coop Pulmonology)

since 2006

“Neutrophil extracellular traps” (NET) in arterial and venous thrombosis and vascular diseases; cytotoxicity of histones