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Role of Semaphorin 7A in regulating vascular and organ integrity during hypoxia and inflammation

Applicant Dr. David Köhler, since 2/2012
Subject Area Anaesthesiology
Term from 2010 to 2014
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 189935024
 
Cellular hypoxia is part of the pathophysiological correlate of an acute inflammatory process. Hypoxia attenuates the epithelial and endothelial barrier function, leading to edema formation and to the extravasation of inflammatory cells, which activation provoke the release of a variety of cytokines. Semaphorin 7A (Sema7A) is a relatively newly identified protein involved in neuronal and immune processes. Its increasing interest lies in the ability to modulate neurite extension, cell migration and to induce the production of cytokines by activation of monocytes and macrophages, actions exerted through interaction with specific α1β1-integrin and Plexin C1 receptors. Our preliminary results demonstrate a novel ability of Sema7A in regulating the inflammatory process during hypoxic conditions. Therefore we propose here to further investigate the regulation of Sema7A expression as well as its specific role in vascular integrity during hypoxia and inflammation. Taken together, with these studies we expect to define novel innate mechanisms to ensure vascular and organ function during conditions of hypoxia and inflammation. Moreover, these findings will help to identify and to develop new experimental therapies that are potentially beneficial to a variety of pathological conditions associated with acute inflammation and hypoxia.
DFG Programme Research Grants
Ehemaliger Antragsteller Julio César Morote Garcia, Ph.D., until 2/2012
 
 

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