Abstract
The physiological functions of lysophosphatidylethanolamine (lysoPE) have not been fully elucidated. In this study, the effects of lysoPE on lipogenesis and lipolysis were investigated in a cultured human liver-derived cell line. The intracellular lipid profile was investigated in detail using liquid chromatography–tandem mass spectrometry (LC-MS/MS) to better understand the underlying mechanism. The expression of genes related to lipid metabolism and catabolism was analyzed using real-time PCR. LysoPE supplementation induced cellular lipid droplet formation and altered triacylglycerol (TAG) profiles. Furthermore, lysoPE downregulated expression of the TAG hydrolyzation regulation factor ATGL, and reduced the expression of fatty acid biosynthesis-related genes SREBP1 and SCD1. LC-MS/MS-based lipidomic profiling revealed that the addition of lysoPE 18:2 increased the PE species containing linoleic acyl, as well as the CE 18:2 species, likely due to the incorporation of linoleic acyl from lysoPE 18:2. Collectively, these findings suggest that lysoPE 18:2 is involved in lipid droplet formation by suppressing lipolysis and fatty acid biosynthesis. Thus, lysoPE might play a pathological role in the induction of fatty liver disease.
Highlights
Academic Editor: Naoki TanakaLysophosphatidylethanolamine is a lysophospholipid that is a deacylated product of phosphatidylethanolamine (PE) hydrolysis induced by phospholipase A1/A2 [1].LysoPE is a minor component of the cell membrane [2] and stimulates chemotactic migration and infiltration of ovarian cancer cells [3]
The present results showed that excessive lipid accumulation induced by lysoPE 18:2 could contribute to the decreased SREBP1 and SCD1 expression, which might be part of a feedback loop that suppresses the intracellular biosynthesis of excess fatty acids
We demonstrated that lysoPE supplementation induced lipid droplet formation in a human liver-derived cell line, and revealed that lysoPE induced increases in TAG, cholesteryl ester (CE), PE, lysoPE and PC, containing linoleic acyl
Summary
Academic Editor: Naoki TanakaLysophosphatidylethanolamine (lysoPE) is a lysophospholipid that is a deacylated product of phosphatidylethanolamine (PE) hydrolysis induced by phospholipase A1/A2 [1].LysoPE is a minor component of the cell membrane [2] and stimulates chemotactic migration and infiltration of ovarian cancer cells [3]. Lysophosphatidylethanolamine (lysoPE) is a lysophospholipid that is a deacylated product of phosphatidylethanolamine (PE) hydrolysis induced by phospholipase A1/A2 [1]. LysoPE functions as a neuronutrient activator through the mitogen-activated protein kinase signaling pathway in pheochromocytoma cells [4]. LysoPE was recently reported to be involved in the stimulation of neurite outgrowth and protection against glutamate toxicity in cultured cortical neurons [5,6]. A previous study showed that lysoPE inhibits lipopolysaccharide-induced M1 macrophage polarization in mouse peritoneal macrophages [7]. The function of lysoPE in the liver has not been reported. Lysophosphatidylcholine (lysoPC) is structurally similar to lysoPE but differs in its headgroup (choline instead of ethanolamine) and is known to form lipid droplets in endothelial cells [8]. Whether lysoPE has a similar effect on liver steatosis remains unknown
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