A Peptied From the NC1 Domain of the α3 Chain of Type IV Collagen Prevents Damage to Basement Membranes by PMN
During the process of acute inflammation, circulating polymorphonuclear leukocytes (PMN) transmigrate from the vascular lumen to the site of infection or injury. This process involves the interaction of PMN with endothelial cells (EC) and subsequent diapedesis of PMN through the subendothelial basement membrane (BM). Along the path of transmigration, PMN come across and interact with numerous macromolecules of BM. Extensive research has been carried out to understand how various components of the C M e.g. type IV Collagen (COL (IV)), laminin, entactin, and proteoglycans mediate the physiological function of PMN (Matzner, Bar-Ner, Yahalom, Ishai-Michaeli, Fuks, and Vlodavsky, 1985; Matzer, Vlodavsky, Michaeli, and Eldor, 1990; Pike, Wicha, Yoon, Mayo, and Boxer, 1989; Senior, Hinek, Griffin, Pipoly, Crouch, and Mecham, 1989; Senior, Gresham, Griffin, Brown, and Chung, 1992). Studies by Huber and Weiss (1989) suggest that the transmigrating PMN cause a transient focal disruption of the BM which allows PMN to traverse it. These disruptions are rapidly repaired by the overlying EC. In our laboratory, the focus has been on the role of COL (IV), a major component of the BMs, on PMN function.
KeywordsCD47 Antigen Alport Syndrome Endothelial Cell Monolayer Collagen Chain Endothelial Cell Growth Medium
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