Abstract
Endothelial cells (EC) are involved in regulating several aspects of lipid metabolism, with recent research revealing the clinicopathological significance of interactions between EC and lipids. Induced pluripotent stem cells (iPSC) have various possible medical uses, so understanding the metabolism of these cells is important. In this study, endothelial phenotype cells generated from human iPSC formed cell networks in co-culture with fibroblasts. Changes of plasmalogen lipids and sphingomyelins in endothelial phenotype cells generated from human iPSC were investigated by reverse-phase ultra-high-pressure liquid chromatography mass spectrometry (UHPLC-MS/MS) analysis. The levels of plasmalogen phosphatidylethanolamines (38:5) and (38:4) increased during differentiation of EC, while sphingomyelin levels decreased transiently. These changes of plasmalogen lipids and sphingomyelins may have physiological significance for EC and could be used as markers of differentiation.
Highlights
Endothelial cells (EC) are multifunctional cells with a role in regulating coagulation and fibrinolysis, vascular tone, angiogenesis, and inflammatory reactions, and EC dysfunction is involved in the pathophysiology of various diseases[1, 2]
EC derived from mouse or human induced pluripotent stem cells were reported in 2008 and 2009 by the same group[9, 10], and it has been shown that cells positive for Flk[1] and VE-cadherin differentiate into EC11
EC derived from induced pluripotent stem cells (iPSC) have the potential for various medical applications[15, 16], but elucidation of the biological features of these cells is required before clinical use can be attempted
Summary
Endothelial cells (EC) are multifunctional cells with a role in regulating coagulation and fibrinolysis, vascular tone, angiogenesis, and inflammatory reactions, and EC dysfunction is involved in the pathophysiology of various diseases[1, 2]. EC derived from mouse or human induced pluripotent stem cells (iPSC) were reported in 2008 and 2009 by the same group[9, 10], and it has been shown that cells positive for Flk[1] ( known as KDR/vascular endothelial growth factor receptor 2, VEGFR2) and VE-cadherin differentiate into EC11. Inhibition of SMS in EC was reported to attenuate lipopolysaccaride (LPS)-induced lung injury in animals through enhancement of the EC barrier by reducing loss of SM from lipid rafts in the cell membrane[27]. Elevated plasma SM levels are a prognostic marker in acute coronary syndrome[28], and overexpression of SMS is suggested to be related to EC dysfunction, a decrease of CD34/KDR-positive endothelial progenitor cells, and development of atherosclerosis in ApoE knock-out mice[29]. Elucidating the behavior of plasmalogens and SM in iPSC-derived EC during differentiation could be helpful for evaluating the potential of medical applications of EC generated from iPSC
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