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Start of funding 01.01.2005
Caveolin signalling in endothelial permeability regulation
Prof. Dr. Detlev Drenckhahn
University of Würzburg
Institute of Anatomy and Cell Biology, Department II
Prof. Dr. Fitz Roy E. Curry
University of California, Davis
Physiology & Membrane Biology
The aim of the new collaboration is to analyze the role of caveolae in NO signalling in endothelial cells. NO is generated by NO synthase (NOS) which is bound by caveolin-1 to caveolae and inhibited in its bound state. Additionally, caveolae are thought to be involved in several other signalling pathways participating in permeability regulation such as protein kinase C. The strength of our collaboration is the combination of single molecule techniques such as laser tweezers and atomic force microscopy on immortalized cultured endothelial cells (Bavarian group) with in vivo studies on animals that are conducted by the California group. By this experimental approach we will focus on how caveolae are involved in permeability regulation via NO and protein kinase C signalling. Using caveolin and NOS knock out mice we have the opportunity to study the role of NO for endothelial permeability regulation in two models with contrary regulation of NOS function. We hope to identify important signalling pathways controlling endothelial permeability that may allow us to develop inhibitors and agonists for treatment of vascular diseases in particular those that are accompanied by increased vascular permeability.