Article
Swiprosin-1 is expressed in mast cells and up-regulated through the protein kinase CβI/η pathway
Article first published online: 19 AUG 2009
DOI: 10.1002/jcb.22307
Copyright © 2009 Wiley-Liss, Inc.
Additional Information
How to Cite
Thylur, R. P., Kim, Y.-D., Kwon, M.-S., Oh, H.-M., Kwon, H.-K., Kim, S.-H., Im, S.-H., Chun, J.-S., Park, Z.-Y. and Jun, C.-D. (2009), Swiprosin-1 is expressed in mast cells and up-regulated through the protein kinase CβI/η pathway. Journal of Cellular Biochemistry, 108: 705–715. doi: 10.1002/jcb.22307
Publication History
- Issue published online: 22 SEP 2009
- Article first published online: 19 AUG 2009
- Manuscript Accepted: 14 JUL 2009
- Manuscript Received: 15 JUN 2009
Funded by
- MEST/KOSEF. Grant Numbers: R01-2008-000-20989-0, R11-2007-007-01002-0
- Korea Research Foundation. Grant Number: 2008-C00265
- Abstract
- Article
- References
- Cited By
Keywords:
- mast cells;
- swiprosin-1;
- protein kinase C;
- calcium
Abstract
Swiprosin-1 exhibits the highest expression in CD8+ T cells and immature B cells and has been thought to play a role in lymphocyte physiology. Here we report that swiprosin-1 is also expressed in mast cells and up-regulated in both in vitro cultured mast cells by phorbol ester and in vivo model tissues of passive cutaneous anaphylaxis and atopic dermatitis. Targeted inhibition of the specific protein kinase C (PKC) isotypes by siRNA revealed that PKC-βI/η are involved in the expression of swiprosin-1 in the human mast cell line HMC-1. In contrast, down-regulation of swiprosin-1 by A23187 or ionomycin suggests that calcium-signaling plays a negative role. The ectopic expression of swiprosin-1 augmented PMA/A23187-induced NF-κB promoter activity, and resulted in increased expression of cytokines. Moreover, knock-down of swiprosin-1 attenuated PMA/A23187-induced cytokine expression. Collectively, these results suggest that swiprosin-1 is a PKC-βI/η-inducible gene and it modulates mast cell activation through NF-κB-dependent pathway. J. Cell. Biochem. 108: 705–715, 2009. © 2009 Wiley-Liss, Inc.

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