As such, endothelial cells harbour specialised rod shaped storage organelles (WPB) that contain multiple pre-made pro-inflammatory and pro-haemostatic proteins. The response to vascular injury or infection is fast this minimises loss of blood and spread of pathogens. An investigation into novel regulatory mechanisms for Von Willebrand factor secretion from endothelial cells My research centres on the mechanisms and machinery required for this intracellular trafficking and the subsequent impact on transmigration of leukocytes through the endothelial cell layer. Some of these adhesion receptors such as Jam-C are known to undergo intracellular trafficking and are found on intracellular vesicles and non-junctional plasma membrane following certain stimuli. The blood vascular endothelium plays a key part in this process as a number of endothelial cell surface receptors such as P- and E-selectin, CD31 and the Junctional Adhesion Molecules (JAMs) have important roles in the recruitment and transmigration of leukocytes through blood-vessel walls. The control of this process is therefore central to a normal resolution of an inflammatory situation. However in some situations inappropriate and excessive recruitment of leukocytes can result in chronically inflamed tissues. Leukocyte recruitment from the blood vascular to infected tissues is a crucial part of the normal inflammatory response and allows clearance of pathogens from the affected area. Trafficking of endothelial tight junction proteins during inflammation Research in my lab centres on the cell biology of endothelial cells during injury and inflammation.Ĭurrently two projects are running in the laboratory: 1.
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