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FEBS Lett. 2015 Aug 4;589(17):2213-7. doi: 10.1016/j.febslet.2015.06.045. Epub 2015 Jul 13.

LPS-mediated septic shock is augmented in ceramide synthase 2 null mice due to elevated activity of TNFα-converting enzyme.

Author information

1
Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel.
2
Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel. Electronic address: tony.futerman@weizmann.ac.il.

Abstract

Tumor necrosis factor α (TNFα) is an inflammatory cytokine that plays an intimate role in septic shock. Injection of high levels of lipopolysaccharide induces septic shock and death in mice within 30 h, whereas ceramide synthase 2 (CerS2) null mice, defective in the synthesis of very-long acyl chain ceramides, die within ∼10 h. The augmented rate of death of CerS2 null mice is due to elevated levels of TNFα secretion as a result of enhanced activity of TNFα-converting enzyme (TACE). We discuss the relationship between the sphingolipid acyl chain length and TACE activity and the relevance of this data to septic shock.

KEYWORDS:

Ceramide; Ceramide synthase 2; LPS-mediated sepsis; Sphingolipid; Tumor necrosis factor α; Tumor necrosis factor α converting enzyme

PMID:
26183206
DOI:
10.1016/j.febslet.2015.06.045
[Indexed for MEDLINE]
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