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GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

ABSTRACT: GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

PROVIDER: PRJNA821058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18516179_1.fastq.gz	Fastqsanger.gz
	SRR18516179_2.fastq.gz	Fastqsanger.gz
	SRR18516180_1.fastq.gz	Fastqsanger.gz
	SRR18516180_2.fastq.gz	Fastqsanger.gz
	SRR18516181_1.fastq.gz	Fastqsanger.gz

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GENE EXPRESION PROFILE OF HEPATIC PROGENITOR CELLS FROM Ptpn1+/+ AND Ptpn1-/- MICE AFTER PALMITIC ACID TREATMENT

Project description:We report the role of PTP1B deficiency in hepatic progenitor cells in the protection against lipotoxic injury

2022-04-01 | GSE199644 | GEO

Upregulated Hepatic Lipogenesis from Dietary Sugars Supplies Palmitic Acid to the Developing Brain of Mice fed Low Palmitic Acid from Birth

Project description:Upregulated Hepatic Lipogenesis from Dietary Sugars Supplies Palmitic Acid to the Developing Brain of Mice fed Low Palmitic Acid from Birth

| PRJNA936413 | ENA

Upregulated Hepatic Lipogenesis from Dietary Sugars Supplies Palmitic Acid to the Developing Brain of Mice fed Low Palmitic Acid from Birth

Project description:Background: Palmitic acid (PAM) can be provided in the diet or synthesized via de novo lipogenesis (DNL) primarily from glucose. Preclinical work on the origin of brain PAM during development is scarce and contrasts results on the origin of adult brain PAM. Here, we utilize naturally occurring carbon isotope ratios (13C/12C; δ13C) and RNA sequencing to uncover the origin of brain PAM, and pathways involved in maintaining brain PAM, respectively, during development. maintaining brain PAM, respectively, during development. Methods: Dams were equilibrated onto diets low (<2%), medium (47%) or high (>95%) in PAM prior to breeding. Dietary PAM was depleted in δ13C, while dietary sugars were enriched. Offspring stayed on the respective dam diet and were euthanized at postnatal day 0, 10, 21, and day 35. Pup liver and brain fatty acids were quantified, after which, tissue δ13C-PAM was measured by compound specific isotope analysis. Day 35 tissue RNA was sequenced on a NovaSeq S4 Flowcell. Results: Although PAM levels in the liver reflected levels of dietary PAM, PAM was maintained in total and individual brain phospholipid fractions across diet groups at all timepoints. Tissue δ13C-PAM was enriched overall and augmented in mice fed low PAM, compared to medium and high PAM suggesting that DNL from dietary sugars maintained the majority of the brain PAM pool. Furthermore, DNL pathways were upregulated in mice fed low compared to high PAM in the liver, but not the brain at day 35. Conclusions: Lipogenesis from dietary sugars maintains the majority of brain PAM during development and is augmented in mice fed low PAM from birth. Importantly, hepatic lipogenesis from dietary sugars determines PAM availability to the developing brain when low in the diet – a compensatory mechanism identified to maintain total brain PAM pools compared to periphery which ultimately suggests an importance of brain PAM regulation during development.

2023-11-08 | GSE225568 | 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 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

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

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.

2021-02-10 | GSE166500 | GEO

Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA

Project description:Transcriptional regulation of genes in AML12 cells treated with Palmitic acid, LXR lingand (GW3965) and Ulk1 siRNA shows differential effect of Ulk1 KD on LXr responsive genes AML-12 cells co-treated with 0.75mM PA+/- 10ÂµM GW3965 for 24 h +/- Ulk1 SiRNA

2016-03-31 | E-GEOD-74059 | biostudies-arrayexpress

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