scholarly journals Lipid droplet formation in response to oleic acid in Huh-7 cells is mediated by the fatty acid receptor FFAR4

2014 ◽  
Vol 127 (14) ◽  
pp. 3104-3115 ◽  
Author(s):  
A. Rohwedder ◽  
Q. Zhang ◽  
S. A. Rudge ◽  
M. J. O. Wakelam
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Acid Receptor ◽  
Lipid Droplet Formation ◽  
Fatty Acid Receptor

Role of hepatic Annexin A6 in fatty acid-induced lipid droplet formation

2017 ◽  
Vol 358 (2) ◽  
pp. 397-410 ◽  
Author(s):  
Rose Cairns ◽  
Anna Alvarez-Guaita ◽  
Inés Martínez-Saludes ◽  
Sundeep J. Wason ◽  
Jacky Hanh ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Lipid Droplet Formation

scholarly journals Retinoic acid receptor-related orphan receptor α reduces lipid droplets by upregulating neutral cholesterol ester hydrolase 1 in macrophages

2019 ◽  
Author(s):  
Hiroshi MATSUOKA ◽  
Riki TOKUNAGA ◽  
Miyu KATAYAMA ◽  
Yuichiro HOSODA ◽  
Kaoruko MIYA ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Lipid Droplet ◽  
Cholesterol Ester ◽  
Retinoic Acid Receptor ◽  
Droplet Formation ◽  
Orphan Receptor ◽  
Acid Receptor ◽  
Cholesterol Ester Hydrolase ◽  
Ester Hydrolase ◽  
Lipid Droplet Formation

Abstract Background: Neutral cholesterol ester hydrolase 1 (NCEH1) catalyzes the hydrolysis of cholesterol ester (CE) in macrophages. Genetic ablation of NCEH1 promotes CE-laden macrophages and the development of atherosclerosis in mice. Dysregulation of NCEH1 levels is involved in the pathogenesis of multiple disorders including metabolic diseases and atherosclerosis; however, relatively little is known regarding the mechanisms regulating NCEH1. Retinoic acid receptor-related orphan receptor α (RORα)-deficient mice exhibit several phenotypes indicative of aberrant lipid metabolism, including dyslipidemia and increased susceptibility to atherosclerosis. Results: In this study, inhibition of lipid droplet formation by RORα positively regulated NCEH1 expression in monocyte-derived macrophages. In mammals, the NCEH1 promoter region was found to harbor putative RORα response elements (ROREs). Electrophoretic mobility shift, chromatin immunoprecipitation, and luciferase reporter assays showed that RORα binds and responds to ROREs in human NCEH1. Moreover, NCEH1 was upregulated through RORα via a phorbol myristate acetate-dependent mechanism during macrophage differentiation from THP1 cells. siRNA-mediated knockdown of RORα significantly downregulated NCEH1 and inhibited lipid droplet formation in human hepatoma cells. In contrast, NCEH1 was induced by treatment with RORα agonists. Conclusion: These data strongly suggested that NCEH1 is a direct RORα target, defining potential new roles for RORα in the inhibition of lipid droplet formation through NCEH1. Keywords: Atherosclerosis, Cholesterol ester, Lipid droplet, Macrophage, Transcriptional regulation, Nuclear receptor, RORα, NCEH1

scholarly journals Retinoic acid receptor-related orphan receptor α reduces lipid droplets by upregulating neutral cholesterol ester hydrolase 1 in macrophages

2020 ◽  
Author(s):  
Hiroshi MATSUOKA ◽  
Riki TOKUNAGA ◽  
Miyu KATAYAMA ◽  
Yuichiro HOSODA ◽  
Kaoruko MIYA ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Lipid Droplet ◽  
Cholesterol Ester ◽  
Lipid Droplets ◽  
Retinoic Acid Receptor ◽  
Droplet Formation ◽  
Orphan Receptor ◽  
Acid Receptor ◽  
Ester Hydrolase ◽  
Lipid Droplet Formation

Abstract Background: Neutral cholesterol ester hydrolase 1 (NCEH1) catalyzes the hydrolysis of cholesterol ester (CE) in macrophages. Genetic ablation of NCEH1 promotes CE-laden macrophages and the development of atherosclerosis in mice. Dysregulation of NCEH1 levels is involved in the pathogenesis of multiple disorders including metabolic diseases and atherosclerosis; however, relatively little is known regarding the mechanisms regulating NCEH1. Retinoic acid receptor-related orphan receptor α (RORα)-deficient mice exhibit several phenotypes indicative of aberrant lipid metabolism, including dyslipidemia and increased susceptibility to atherosclerosis. Results: In this study, inhibition of lipid droplet formation by RORα positively regulated NCEH1 expression in macrophages. In mammals, the NCEH1 promoter region was found to harbor putative RORα response elements (ROREs). Electrophoretic mobility shift, chromatin immunoprecipitation, and luciferase reporter assays showed that RORα binds and responds to ROREs in human NCEH1. Moreover, NCEH1 was upregulated through RORα via a phorbol myristate acetate-dependent mechanism during macrophage differentiation from THP1 cells. siRNA-mediated knockdown of RORα significantly downregulated NCEH1 expression and accumulated lipid droplets in human hepatoma cells. In contrast, NCEH1 expression and removal of lipid droplets were induced by RORα agonist treatments and RORα overexpression in macrophages. Conclusion: These data strongly suggested that NCEH1 is a direct RORα target, defining potential new roles for RORα in the inhibition of lipid droplet formation through NCEH1.

scholarly journals Retinoic acid receptor-related orphan receptor α reduces lipid droplets by upregulating neutral cholesterol ester hydrolase 1 in macrophages

2020 ◽  
Author(s):  
Hiroshi MATSUOKA ◽  
Riki TOKUNAGA ◽  
Miyu KATAYAMA ◽  
Yuichiro HOSODA ◽  
Kaoruko MIYA ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Lipid Droplet ◽  
Cholesterol Ester ◽  
Lipid Droplets ◽  
Retinoic Acid Receptor ◽  
Droplet Formation ◽  
Orphan Receptor ◽  
Acid Receptor ◽  
Ester Hydrolase ◽  
Lipid Droplet Formation

Abstract Background: Neutral cholesterol ester hydrolase 1 (NCEH1) catalyzes the hydrolysis of cholesterol ester (CE) in macrophages. Genetic ablation of NCEH1 promotes CE-laden macrophages and the development of atherosclerosis in mice. Dysregulation of NCEH1 levels is involved in the pathogenesis of multiple disorders including metabolic diseases and atherosclerosis; however, relatively little is known regarding the mechanisms regulating NCEH1. Retinoic acid receptor-related orphan receptor α (RORα)-deficient mice exhibit several phenotypes indicative of aberrant lipid metabolism, including dyslipidemia and increased susceptibility to atherosclerosis. Results: In this study, inhibition of lipid droplet formation by RORα positively regulated NCEH1 expression in macrophages. In mammals, the NCEH1 promoter region was found to harbor putative RORα response elements (ROREs). Electrophoretic mobility shift, chromatin immunoprecipitation, and luciferase reporter assays showed that RORα binds and responds to ROREs in human NCEH1. Moreover, NCEH1 was upregulated through RORα via a phorbol myristate acetate-dependent mechanism during macrophage differentiation from THP1 cells. siRNA-mediated knockdown of RORα significantly downregulated NCEH1 expression and accumulated lipid droplets in human hepatoma cells. In contrast, NCEH1 expression and removal of lipid droplets were induced by RORα agonist treatments and RORα overexpression in macrophages. Conclusion: These data strongly suggested that NCEH1 is a direct RORα target, defining potential new roles for RORα in the inhibition of lipid droplet formation through NCEH1.

Seipin deficiency alters fatty acid Δ9 desaturation and lipid droplet formation in Berardinelli-Seip congenital lipodystrophy

Biochimie ◽  
2009 ◽  
Vol 91 (6) ◽  
pp. 796-803 ◽  
Author(s):  
Emilie Boutet ◽  
Haquima El Mourabit ◽  
Matthieu Prot ◽  
Mona Nemani ◽  
Eliane Khallouf ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Lipid Droplet Formation

Flow cytometric analysis of lipid droplet formation in cells of the human monocytic cell line, U937

1991 ◽  
Vol 69 (8) ◽  
pp. 571-576 ◽  
Author(s):  
K. Suzuki ◽  
N. Sakata ◽  
M. Hara ◽  
A. Kitani ◽  
M. Harigai ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cell Line ◽  
Lipid Droplet ◽  
Droplet Formation ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Human Monocytic Cell Line ◽  
Lipid Droplet Formation ◽  
Human Monocytic Cell

Active uptake of a free fatty acid, oleate, and its incorporation into triacylglycerol and phospholipid in the human monocytic cell line, U937, was identified using 14C-labelled oleate. Excess triacylglycerol accumulates in the form of lipid droplets in the cytoplasm. The extent of lipid droplet formation in each cell can be assessed in the absence of any staining by 90° light scatter intensity, one of the basic parameters of flow cytometry.Key words: monocyte, free fatty acid, triacylglycerol, flow cytometry.

scholarly journals Retinoic acid receptor-related orphan receptor α reduces lipid droplets by upregulating neutral cholesterol ester hydrolase 1 in macrophages

2020 ◽  
Author(s):  
Hiroshi MATSUOKA ◽  
Riki TOKUNAGA ◽  
Miyu KATAYAMA ◽  
Yuichiro HOSODA ◽  
Kaoruko MIYA ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Lipid Droplet ◽  
Cholesterol Ester ◽  
Lipid Droplets ◽  
Retinoic Acid Receptor ◽  
Droplet Formation ◽  
Orphan Receptor ◽  
Acid Receptor ◽  
Ester Hydrolase ◽  
Lipid Droplet Formation

Abstract Background: Neutral cholesterol ester hydrolase 1 (NCEH1) catalyzes the hydrolysis of cholesterol ester (CE) in macrophages. Genetic ablation of NCEH1 promotes CE-laden macrophages and the development of atherosclerosis in mice. Dysregulation of NCEH1 levels is involved in the pathogenesis of multiple disorders including metabolic diseases and atherosclerosis; however, relatively little is known regarding the mechanisms regulating NCEH1. Retinoic acid receptor-related orphan receptor α (RORα)-deficient mice exhibit several phenotypes indicative of aberrant lipid metabolism, including dyslipidemia and increased susceptibility to atherosclerosis. Results: In this study, inhibition of lipid droplet formation by RORα positively regulated NCEH1 expression in macrophages. In mammals, the NCEH1 promoter region was found to harbor putative RORα response elements (ROREs). Electrophoretic mobility shift, chromatin immunoprecipitation, and luciferase reporter assays showed that RORα binds and responds to ROREs in human NCEH1. Moreover, NCEH1 was upregulated through RORα via a phorbol myristate acetate-dependent mechanism during macrophage differentiation from THP1 cells. siRNA-mediated knockdown of RORα significantly downregulated NCEH1 expression and accumulated lipid droplets in human hepatoma cells. In contrast, NCEH1 expression and removal of lipid droplets were induced by RORα agonist treatments and RORα overexpression in macrophages. Conclusion: These data strongly suggested that NCEH1 is a direct RORα target, defining potential new roles for RORα in the inhibition of lipid droplet formation through NCEH1.

ADRP stimulates lipid accumulation and lipid droplet formation in murine fibroblasts

2002 ◽  
Vol 283 (4) ◽  
pp. E775-E783 ◽  
Author(s):  
Minako Imamura ◽  
Toyoshi Inoguchi ◽  
Shoichiro Ikuyama ◽  
Susumu Taniguchi ◽  
Kunihisa Kobayashi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Droplet ◽  
Lipid Accumulation ◽  
Lipid Droplets ◽  
Droplet Formation ◽  
Fatty Acid Binding ◽  
Lipogenic Genes ◽  
Lipid Droplet Formation ◽  
Murine Fibroblasts ◽  
Adipose Differentiation

Adipose differentiation-related protein (ADRP) is a lipid droplet-associated protein that is expressed early during adipose differentiation. The present study was undertaken to reveal the role of ADRP in adipose differentiation. In murine fibroblasts infected with green fluorescent protein (GFP)-ADRP fusion protein expression adenovirus vector, confocal microscopic analysis showed the number and size of lipid droplets apparently increased comparing with those of control cells. Overexpressed GFP-ADRP were mainly located at the surface of lipid droplets and appeared to be “ring-shaped.” Triacylglycerol content was also significantly ( P < 0.001) increased in GFP-ADRP-overexpressed cells compared with control cells. ADRP-induced lipid accumulation did not depend on adipocyte-specific gene induction, such as peroxisome proliferator-activated receptor-γ, lipoprotein lipase, or other lipogenic genes, including acyl-CoA synthetase, fatty acid-binding protein, and fatty acid transporter. In conclusion, ADRP stimulated lipid accumulation and lipid droplet formation without induction of other adipocyte-specific genes or other lipogenic genes in murine fibroblasts. The detailed molecular mechanisms of ADRP on lipid accumulation remain to be elucidated.

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