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(Journal of Leukocyte Biology. 2002;71:223-230.)
© 2002 by Society for Leukocyte Biology

Monocyte cell adhesion induced by a human aminoacyl-tRNA synthetase-associated factor, p43: identification of the related adhesion molecules and signal pathways

Heonyong Park, Sang Gyu Park, Joong-Won Lee, Taeho Kim, Gyuyoup Kim, Young-Gyu Ko and Sunghoon Kim

National Creative Research Initiatives Center for ARS Network, College of Pharmacy, Seoul National University, Korea

Correspondence: Sunghoon Kim, National Creative Research Initiatives Center for ARS Network, College of Pharmacy, Seoul National University, San 56-1, Shillim-dong, Kwanak-ku, Seoul, 151-742, Korea. E-mail: sungkim{at}snu.ac.kr

An aminoacyl-tRNA synthetase-associated factor, p43, was recently shown to be secreted to induce a proinflammatory response. Because a proinflammatory response involves the cell-cell adhesion between endothelial and immune cells, we first examined the mechanism of p43-induced cell-cell adhesion of myelomonocytic leukemia cells. Intercellular adhesion molecule-1 (ICAM-1) was up-regulated by p43 and mediated p43-induced cell-cell adhesion via the interaction with LFA-1 or Mac-1. We also investigated p43-stimulated signaling pathways involved in the homotypic THP-1 cell adhesion. Because the specific inhibitors for PI3-K (phosphatidylinositol 3-kinase), ERK (extracellular signal-regulating kinase), and p38 MAPK (mitogen-activated protein kinase) blocked p43-stimulated ICAM-1 expression and homotypic THP-1 cell adhesion, these kinases were responsible for p43-induced cell-cell adhesion. p43-Dependent activation of ERK was inhibited by PI3-K inhibitors, and the activation of p38 MAPK was not. Thus, the results of this work suggest that p43 should induce cell-cell adhesion via the PI3-K/ERK- and p38 MAPK-dependent up-regulation of ICAM-1.

Key Words: intercellular adhesion molecule-1 • mitogen-activated protein kinase • cell-cell adhesion • integrin ß2




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