In human macrophages the complement component C5a induces the expression of oncostatin M via AP-1 activation

44Citations
Citations of this article
30Readers
Mendeley users who have this article in their library.

Abstract

Objective: Macrophages produce the cytokine oncostatin M (OSM), which beside other functions is also involved in inflammation. The complement component C5a mobilizes and activates these cells at inflammatory sites. We examined the effect of C5a on OSM production in human monocytes and in human monocyte-derived macrophages. Methods and Results: For macrophage transformation peripheral blood monocytes were cultivated for 8 to 10 days in the presence of human serum. C5a significantly increased in these cells OSM antigen as determined by specific ELISA and mRNA as quantitated by real-time polymerase chain reaction in these cells as well as in plaque macrophages. This effect was blocked by antibodies against the receptor C5aR/CD88 and by pertussis toxin. The C5a-induced phosphorylation of p38 and JNK and the C5a-induced increase in OSM production in macrophages was abolished by 2 p38 inhibitors and by a JNK inhibitor. Furthermore C5a increased the nuclear translocation of c-fos and c-jun. Using different OSM promoter deletion mutant constructs we show that the putative AP-1 element is responsible for activation of OSM promoter activity by C5a. Conclusion: Our data establish a link between the complement system and the gp130 receptor cytokine family with possible implications for the pathology of inflammatory diseases. © 2008 American Heart Association, Inc.

Cite

CITATION STYLE

APA

Kastl, S. P., Speidl, W. S., Kaun, C., Katsaros, K. M., Rega, G., Afonyushkin, T., … Wojta, J. (2008). In human macrophages the complement component C5a induces the expression of oncostatin M via AP-1 activation. Arteriosclerosis, Thrombosis, and Vascular Biology, 28(3), 498–503. https://doi.org/10.1161/ATVBAHA.107.160580

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free