Role of beta1-integrin signaling in lymphatic vessel formation

• Applicant: Professor Dr. Eckhard Lammert
• Subject Area: Developmental Biology
• Term: from 2011 to 2014
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 192924567

Fluid leaks out of most vascular beds and increases the interstitial fluid pressure within a given tissue. Therefore, lymphatic vessels absorb this fluid and bring it back to the vascular system. This process is mediated by an interaction of lymphatic endothelial cells with the extracellular matrix (ECM) that opens the lymphatic vessels, whenever the interstitial fluid pressure rises. However, even though lymphatic endothelial cells express many beta1-integrin receptors for ECM proteins, little is known about the in vivo role of the beta1-integrin in lymphatic vessels. Thus we want to investigate the beta1-integrin and its signaling pathway in lymphatic vessels by using mice that lack the beta1-integrin and integrin-linked kinase (ILK) in their endothelial cells. Our current work warrants this study by showing that beta1-integrin deficient mice have severe defects in lymphatic vessel formation. We also plan to analyze how beta1-integrin and ILK regulate VEGF receptor-3 signaling in lymphatic endothelial cells in vitro and in vivo.

• DFG Programme: Research Grants