Effects of S100A8/A9 on Inflammation in Atherosclerosis
Author Information
Author(s): Ehlermann Philipp, Eggers Kai, Bierhaus Angelika, Most Patrick, Weichenhan Dieter, Greten Johannes, Nawroth Peter P, Katus Hugo A, Remppis Andrew
Primary Institution: Universität Heidelberg
Hypothesis
The study aims to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.
Conclusion
Heterodimeric S100A8/S100A9 may play a significant role in triggering atherosclerosis in diabetes and renal failure, suggesting it could be a target for new treatments.
Supporting Evidence
- Heterodimeric S100A8/S100A9 enhanced secretion of proinflammatory cytokines in a dose-dependent manner.
- The effects of S100A8/S100A9 were not observed with homodimeric proteins.
- Inhibition of MAP-kinase pathways reduced the effects of S100A8/S100A9.
- AGE preincubation sensitized endothelial cells to the effects of S100A8/S100A9.
Takeaway
This study found that a specific protein complex can make blood vessel cells more inflamed, which might help explain heart problems in people with diabetes.
Methodology
Human umbilical vein endothelial cells were preincubated with AGE-albumin and then stimulated with S100A8/S100A9 to measure inflammatory responses.
Limitations
The study did not include control experiments using soluble RAGE to assess RAGE-specific effects.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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