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

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

PROVIDER: PRJNA666670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12748727_1.fastq.gz	Fastqsanger.gz
	SRR12748727_2.fastq.gz	Fastqsanger.gz
	SRR12748728_1.fastq.gz	Fastqsanger.gz
	SRR12748728_2.fastq.gz	Fastqsanger.gz
	SRR12748729_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2021-01-18 | GSE158834 | GEO

Effect of palmitic acid on gene expression of two types of endothelial cells

Project description:To investigate the effect of palmitic acid on gene expression of rat corpus cavernosum endothelial cells (RCCECs) and human umbilical vein endothelial cells (HUVECs), we used palmitic acid to treat these two primary cells, which were then subjected to RNA-seq.

2022-12-01 | GSE205913 | GEO

Effect of exogenous FABP4 (A-FABP/aP2) with and without palmitic acid on gene expression in RAW264.7 macrophages

Project description:Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4. RAW264.7 macrophages were treated with and without 200 nM recombinant FABP4 in the absence and presence of 0.2 mM palmitic acid.

2015-09-19 | E-GEOD-73173 | biostudies-arrayexpress

Effect of Palmitic acid on the transcriptional profile of skin regulatory T cells (Tregs)

Project description:We found that palmitic acid inhibits proliferation and cell death of Tregs in the skin. The goal of this study is to investigate how Palmitic acid drives lipid toxicity in skin Tregs

2023-07-01 | GSE208210 | GEO

Abnormal metabolism of palmitic acid promotes the formation of renal calcium oxalate stones

Project description:Individual metabolic factors are involved in the occurrence and development of CaOx stones, and dyslipidemia is an independent risk factor for the formation of urolithiasis. This study have screened out palmitic acid as one of the significantly differential metabolites in the urine of patients with renal CaOx stones compared with healthy controls by metabolomics. This study aims to further clarify the correlation between abnormal palmitic acid metabolism and the formation of renal CaOx stones, confirm the promoting effect of abnormal palmitic acid metabolism on the adhesion of CaOx crystals and the formation of renal CaOx stones

2024-02-21 | GSE240279 | GEO

Palmitic acid regulates the biological function of Ovarian Cancer

Project description:Palmitic acid was positively correlated with the invasion ability of ovarian cancer cells, its up-regulation inhibited the migrative, invasive and cloning capacity of cancer cells in vitro and suppressed the tumor proliferation and intraperitoneal diffusion in vivo, while its up-regulation did the opposite.

2024-12-17 | GSE279101 | GEO

Palmitic Acid Upregulates Type I Interferon-Mediated Antiviral Response and Cholesterol Biosynthesis in Human Astrocytes

Project description:Chronic intake of a high-fat diet increases saturated fatty acids in the brain causing the progression of neurodegenerative diseases. Palmitic acid is a free fatty acid abundant in the diet that at high concentrations may penetrate the blood brain barrier and stimulate the production of pro-inflammatory cytokines, leading to inflammation in astrocytes. The use of the synthetic neurosteroid tibolone in protection against fatty acid toxicity is emerging, but its transcriptional effects on palmitic acid induced lipotoxicity remain unclear. Herein, we performed a transcriptome profiling of normal human astrocytes to investigate the molecular mechanisms by which palmitic acid causes cellular damage to astrocytes, and whether tibolone could reverse its detrimental effects. Astrocytes undergo a profound transcriptional change at 2 mM palmitic acid, affecting the expression of 739 genes, 366 upregulated and 373 downregulated. However, tibolone at 10 nM does not entirely reverse palmitic acid effects. Additionally, the protein protein interaction reveals two novel gene clustering modules. The first module involves astrocyte defense responses by upregulation of pathways associated with antiviral innate immunity, and the second is linked to lipid metabolism. Our data suggest that activation of viral response signaling pathways might be so far, the initial molecular mechanism of astrocytes in response to a lipotoxic insult by palmitic acid, triggered particularly upon increased expression levels of *IFIT2*, *IRF1*, and *XAF1*. Therefore, this novel approach using a global gene expression analysis may shed light on the pleiotropic effects of palmitic acid on astrocytes, and provide a basis for future studies addressed to elucidate these responses in neurodegenerative conditions, which is highly valuable for the design of therapeutic strategies.

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Gene expression profiling of C57BL/6 mouse lung tissue with various treatments

Project description:This SuperSeries is composed of the following subset Series: GSE36420: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA07 array GSE36421: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA10 array GSE36422: Gene expression profiling of C57BL/6 mouse lung tissue with various treatments using the MA11 array Refer to individual Series

2012-03-14 | E-GEOD-36423 | biostudies-arrayexpress

Gene expression data from differentiated 3T3-L1 preadipocytes treated with Palmitic Acid, Stearic Acid, Palmitoleic Acid, or Oleic Acid

Project description:Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA). Global gene expression was examined in differentiated preadipocytes treated with either 250 M-NM-<M PA, SA, PMA, or OA for 48 hrs. Individual fatty acid treatments had significant effects on adipocyte gene expression. Functional analyses revealed that PA induced the TLR signalling pathway, while PMA had the opposite effect. SA and OA had similar effects, with increases in key metabolic pathways including mTOR and PPAR signalling, and a reduction in TLR signalling. Ccl5 was validated as a candidate gene that may mediate the differential inflammatory effects of SFA and MUFA in AT. Individual SFA and MUFA trigger distinct transcriptional responses in differentiated preadipocytes, with inflammatory and metabolic pathways particularly sensitive to these fatty acids. A total of 4 microarrays were run for each FA treatment. We experienced difficulties with the cRNA amplification for one replicate from the OA treated cells; therefore this treatment group only had an n=3. For each sample, 100 ng of total RNA was prepared for hybridization to Affymetrix Mouse Gene 1.1 ST array strips, according to the manufacturerM-bM-^@M-^Ys instructions (Affymetrix Inc., Fremont, CA, USA).

2012-11-13 | E-GEOD-42220 | biostudies-arrayexpress

Nascent RNA sequencing (PRO-seq) after various treatments in T47D cells

Project description:Nascent RNA sequencing (PRO-seq) after various treatments in T47D cells

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