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[B. Cell Biology/Stem Cell] B-26



                JAM-A function in flow dependent vascular inflammation




                                                    Jenita Immanuel¹

                                  ¹Biotechnology, Inje University, Gimhae Gimhae - Si, Korea





        Endothelial JAM-A contributes to tight junction formation, but when released from lateral domains, moves to other
        regions where it mediates leukocyte adhesion and contributes to angiogenesis and atherosclerosis. Inflammatory

        ligands or disturbed flow induces re-localization of JAM-A from tight junction to the luminal surface to mediate
        leukocyte binding. Recent phospho-proteomic analysis revealed that JAM-A S285 phosphorylation is decreased on

        fibronectin  compared  to  basement  membrane  protein.  In  addition,  genetic  deletion  of  JAM-A  in  bovine  aortic
        endothelial cells plated on fibronectin led to reduced disturbed flow-induced monocyte adhesion. These results

        suggest that fibronectin may facilitate flow-induced vascular inflammation by JAM-A S285 dephosphorylation.
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