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IL-27 inhibits lymphatic endothelial cell proliferation by STAT1-regulated gene expression
Sebastian Rune Nielsen1, Troels Hammer, Josefine Gibson
1Faculty of Health Sciences, Department of Cellular and Molecular Medicine, Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.
Microcirculation (New York, N.Y. : 1994)
|March 5, 2013
Summary
Interleukin-27 (IL-27) inhibits lymphatic endothelial cell proliferation by activating STAT1 and up-regulating chemokines, revealing its role as an anti-lymphangiogenic regulator.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Interleukin-27 (IL-27) is a cytokine in the IL-12 family.
- IL-27 influences T-helper cell differentiation and inhibits tumor angiogenesis.
- The lymphatic system's development involves interactions with the immune system.
Purpose of the Study:
- To investigate the effect of IL-27 on lymphatic endothelial cell (LEC) proliferation.
- To understand the interplay between the immune system and lymphatic system development.
Main Methods:
- Western blotting and RT-PCR to measure signal transduction and chemokine synthesis (CXCL10, CXCL11) in IL-27-stimulated human dermal LECs.
- MTT and BrdU assays for proliferation analysis.
- siRNA and recombinant proteins to determine the roles of STAT1 and chemokines.
Main Results:
- IL-27 induced JAK-dependent STAT1 and STAT3 phosphorylation in LECs.
- IL-27 inhibited LEC proliferation and migration.
- IL-27 significantly upregulated CXCL10 and CXCL11 expression; these chemokines inhibited FGF-2-induced proliferation.
- STAT1 knockdown abrogated IL-27-induced chemokine expression and proliferation inhibition.
Conclusions:
- IL-27 acts as an anti-lymphangiogenic regulator in vitro.
- IL-27 up-regulates chemokines (CXCL10, CXCL11) via STAT1 activation.
- IL-27 interferes with growth factor-induced proliferation in lymphatic endothelial cells.
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