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Induction of JAM-A during differentiation of human THP-1 dendritic cells
Noriko Ogasawara1, Takashi Kojima, Mitsuru Go
1Department of Otolaryngology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo, Japan.
Insights
Junctional adhesion molecule A (JAM-A) expression increases during dendritic cell (DC) differentiation from human monocytes. This JAM-A upregulation is independent of PPAR-gamma and the p38 MAPK pathway.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Junctional adhesion molecule A (JAM-A) is expressed on endothelial, epithelial cells, and circulating immune cells like leukocytes and dendritic cells (DCs).
- Understanding the regulation of JAM-A in DCs is crucial for comprehending immune cell interactions and functions.
Purpose of the Study:
- To investigate the regulation of JAM-A expression during the differentiation of human monocytic THP-1 cells into mature dendritic cells (DCs).
- To determine the role of Peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonists in modulating JAM-A expression and DC morphology.
Main Methods:
- Differentiated mature DCs from human monocytic THP-1 cells using IL-4, GM-CSF, TNF-alpha, and ionomycin.
- Analyzed mRNA expression of tight junction molecules, including JAM-A, in monocytes and mature DCs via RT-PCR.
- Investigated the effect of PPAR-gamma agonists on DC differentiation and JAM-A expression.
Main Results:
- mRNA and protein levels of JAM-A were significantly increased in mature DCs compared to THP-1 monocytes.
- PPAR-gamma agonists inhibited dendrite elongation in mature DCs but did not affect the upregulation of JAM-A.
- The induction of JAM-A during DC differentiation was found to be independent of PPAR-gamma and the p38 MAPK pathway.
Conclusions:
- JAM-A expression is significantly induced during the differentiation of human THP-1 cells into mature dendritic cells.
- The observed increase in JAM-A is independent of PPAR-gamma signaling and the p38 MAPK pathway.
- These findings provide insights into the molecular mechanisms regulating JAM-A in dendritic cells.
Abstract:
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-alpha, and ionomycin, and some cells were pretreated with the PPAR-gamma 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-gamma 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-gamma and the p38 MAPK pathway.
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