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Published on: August 25, 2013
Sphingomyelin synthase 2 deficiency attenuates NFkappaB activation.
Tiruneh K Hailemariam1, Chongmin Huan, Jing Liu
1Department of Anatomy and Cell Biology, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|June 21, 2008
Summary
Sphingomyelin synthase 2 (SMS2) regulates nuclear factor kappa B (NFkappaB) activation, a key factor in atherosclerosis. SMS2 deficiency reduces NFkappaB activation, suggesting a role in preventing proatherogenic processes.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Nuclear factor kappa B (NFkappaB) is a proatherogenic factor regulating proinflammatory genes.
- Sphingomyelin (SM) metabolism influences NFkappaB activation, but mechanisms are unclear.
- SMS2 impacts SM levels and may regulate NFkappaB.
Purpose of the Study:
- Investigate the role of SMS2 in NFkappaB activation.
- Determine SMS2's influence on atherosclerosis-related pathways.
Main Methods:
- Utilized SMS2 knockout (KO) mice macrophages and SMS2 siRNA-treated HEK 293 cells.
- Stimulated cells with lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha).
- Assessed NFkappaB activation, target gene expression, receptor complex levels, and lipid raft recruitment.
Main Results:
- NFkappaB activation and target gene expression were attenuated in SMS2-deficient cells.
- SMS2 deficiency reduced toll-like receptor 4 (TLR4)-MD2 complex levels post-LPS.
- SMS2 deficiency altered sphingomyelin, diacylglycerol, and ceramide levels, impacting lipid rafts.
Conclusions:
- SMS2 modulates NFkappaB activation.
- SMS2 plays a role in the NFkappaB-mediated proatherogenic process.
- Targeting SMS2 may offer therapeutic strategies for atherosclerosis.
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