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Induction of JAM-A during differentiation of human THP-1 dendritic cells

Junctional adhesion molecule (JAM)-A is not only localized at tight junctions of endothelial and epithelial cells but is also expressed on circulating leukocytes and dendritic cells (DCs). In the present study, to investigate the regulation of JAM-A in DCs, mature DCs were differentiated from the hu...

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Published in:Biochemical and biophysical research communications 2009-11, Vol.389 (3), p.543-549
Main Authors: Ogasawara, Noriko, Kojima, Takashi, Go, Mitsuru, Fuchimoto, Jun, Kamekura, Ryuta, Koizumi, Jun-ichi, Ohkuni, Tsuyoshi, Masaki, Tomoyuki, Murata, Masaki, Tanaka, Satoshi, Ichimiya, Shingo, Himi, Tetsuo, Sawada, Norimasa
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Language:English
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Summary:Junctional adhesion molecule (JAM)-A is not only localized at tight junctions of endothelial and epithelial cells but is also expressed on circulating leukocytes and dendritic cells (DCs). In the present study, to investigate the regulation of JAM-A in DCs, mature DCs were differentiated from the human monocytic cell THP-1 by treatment with IL-4, GM-CSF, TNF-α, and ionomycin, and some cells were pretreated with the PPAR-γ agonists. In the THP-1 monocytes, mRNAs of tight junction molecules, occludin, tricellulin, JAM-A, ZO-1, ZO-2 and claudin-4, -7, -8, and -9 were detected by RT-PCR. In mature DCs that had elongated dendrites, mRNA and protein of JAM-A were significantly increased compared to the monocytes. PPAR-γ agonists prevented the elongation of dentrites but not upregulation of JAM-A in mature DCs. These findings indicated that the induction of JAM-A occurred during differentiation of human THP-1 DCs and was independent of PPAR-γ and the p38 MAPK pathway.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.09.024