Page 52 - ebook

[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.