Sphingosine kinase 1 is required for myristate-induced TNFα expression in intestinal epithelial cells

Publication date: Available online 29 January 2020Source: Prostaglandins & Other Lipid MediatorsAuthor(s): Songhwa Choi, Justin M. Snider, Chris P. Cariello, Johana M. Lambert, Andrea K. Anderson, L. Ashley Cowart, Ashley J. SniderAbstractSaturated fatty acids (SFA) have been known to trigger inflammatory signaling in metabolic tissues; however, the effects of specific SFAs in the intestinal epithelium have not been well studied. Several previous studies have implicated disruption in sphingolipid metabolism by oversupply of SFAs could affect the inflammatory process. Also, our previous studies have implicated sphingosine kinase 1 (SK1) and its product sphingosine-1-phosphate (S1P) as having key roles in the regulation of inflammatory processes in the intestinal epithelium. Therefore, to define the role for specific SFAs in inflammatory responses in intestinal epithelial cells, we examined myristate (C14:0) and palmitate (C16:0). Myristate, but not palmitate, significantly induced pro-inflammatory cytokine tumor necrosis factor α (TNFα), and it was SK1-dependent. Interestingly, myristate-induced TNFα expression was not suppressed by inhibition of S1P receptors (S1PRs), hinting at a potential novel intracellular target of S1P. Additionally, myristate regulated the expression of TNFα via JNK activation in an SK1-dependent manner, suggesting a novel S1PR-independent target as a mediator between SK1 and JNK in response to myristate. Lastly, a myristate-enriched milk fat-based ...
Source: Prostaglandins and Other Lipid Mediators - Category: Lipidology Source Type: research
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