GSE158834: RNA sequencing of ADIPOR2 knockout HEK293 cells undergone various treatments with palmitic acid

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GROUP CONDITION SAMPLES
HEK293 ADIPOR2 Knocko
GSM4811781 GSM4811782 GSM4811783
GSM4811784 GSM4811785 GSM4811786 GSM4811787 GSM4811788 GSM4811789 GSM4811790 GSM4811791 GSM4811792
GSM4811793 GSM4811794 GSM4811795 GSM4811796 GSM4811797 GSM4811798 GSM4811799 GSM4811800 GSM4811801
HEK293 ADIPOR2 Wildty
GSM4811760 GSM4811761 GSM4811762
GSM4811763 GSM4811764 GSM4811765 GSM4811766 GSM4811767 GSM4811768 GSM4811769 GSM4811770 GSM4811771
GSM4811772 GSM4811773 GSM4811774 GSM4811775 GSM4811776 GSM4811777 GSM4811778 GSM4811779 GSM4811780
Description

Submission Date: Sep 30, 2020

Summary: How cells maintain vital membrane lipid homeostasis while obtaining most of their constituent fatty acids from a varied diet remains largely unknown. Here, we used transcriptomics, lipidomics, growth and respiration assays and membrane property analyses in human HEK293 cells or human umbilical vein endothelial cells (HUVEC) to show that the function of AdipoR2 is to respond to membrane rigidification by regulating many lipid metabolism genes. We also show that AdipoR2-dependent membrane homeostasis is critical for growth and respiration in cells challenged with saturated fatty acids. Additionally, we found that AdipoR2 deficiency causes transcriptome and cell physiological defects similar to those observed in SREBP-deficient cells upon SFA challenge. Finally, we compared several genes considered important for lipid homeostasis, namely AdipoR2, SCD, FADS2, PEMT and ACSL4, and found that AdipoR2 and SCD are the most important among these to prevent membrane rigidification and excess saturation when human cells are challenged with exogenous SFAs. We conclude that AdipoR2-dependent membrane homeostasis is especially important for the non-toxic uptake of SFAs.

GEO Accession ID: GSE158834

PMID: 33444759

Description

Submission Date: Sep 30, 2020

Summary: How cells maintain vital membrane lipid homeostasis while obtaining most of their constituent fatty acids from a varied diet remains largely unknown. Here, we used transcriptomics, lipidomics, growth and respiration assays and membrane property analyses in human HEK293 cells or human umbilical vein endothelial cells (HUVEC) to show that the function of AdipoR2 is to respond to membrane rigidification by regulating many lipid metabolism genes. We also show that AdipoR2-dependent membrane homeostasis is critical for growth and respiration in cells challenged with saturated fatty acids. Additionally, we found that AdipoR2 deficiency causes transcriptome and cell physiological defects similar to those observed in SREBP-deficient cells upon SFA challenge. Finally, we compared several genes considered important for lipid homeostasis, namely AdipoR2, SCD, FADS2, PEMT and ACSL4, and found that AdipoR2 and SCD are the most important among these to prevent membrane rigidification and excess saturation when human cells are challenged with exogenous SFAs. We conclude that AdipoR2-dependent membrane homeostasis is especially important for the non-toxic uptake of SFAs.

GEO Accession ID: GSE158834

PMID: 33444759

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