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Related Experiment Video

Updated: Jun 29, 2026

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds

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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.

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Published on: December 9, 2022

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.