FITM2 Deficiency Promotes Hepatic ER Stress in Vitro and in Vivo
- Description
This study examined the role of hepatic FITM2, an endoplasmic reticulum (ER) protein, in the partitioning of newly-synthesized triglyceride between the ER, lipid droplets, and nascent very low density lipoprotein (VLDL) particles in vitro and in vivo. The experiments were conducted using a rat hepatic cell line (McA cells) and mice. Effects of FITM2 deficiency on VLDL assembly and secretion in vitro and in vivo were measured by multiple methods, including density gradient ultracentrifugation, chromatography, mass spectrometry, stimulated Raman scattering microscopy, sub-cellular fractionation, immunoprecipitation, immunofluorescence, and electron microscopy. The dataset contains source data for underlying figures, which includes data on FITM2-deficiency decreases hepatic triglyceride secretion and the density of VLDL particles, FITM2-deficiency promotes lipids accumulation in the ER of cultured hepatic cells, effects of liver-specific FITM2-deficiency on plasma and hepatic triglyceride metabolism and apoB100-lipoprotein density, and hepatic FITM2-deficiency in lipid-loaded hepatic cells results in ER stress both in vitro and in vivo.
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Application RequiredAuthor Approval Required
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- Grant Support
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Howard Hughes Medical Institute/Howard Hughes Medical Institute19POST34410063/American Heart AssociationALF Liver Scholar Award/American Liver Foundation