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Hexokinase 2 Exacerbates Mitochondrial Damage, Neuroinflammation, and Lipid accumulation by promoting ACSL4 ISGylation in Sepsis-Associated Encephalopathy

ABSTRACT: Hexokinase 2 Exacerbates Mitochondrial Damage, Neuroinflammation, and Lipid accumulation by promoting ACSL4 ISGylation in Sepsis-Associated Encephalopathy

PROVIDER: PRJNA1180095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31174461_1.fastq.gz	Fastqsanger.gz
	SRR31174461_2.fastq.gz	Fastqsanger.gz
	SRR31174462_1.fastq.gz	Fastqsanger.gz
	SRR31174462_2.fastq.gz	Fastqsanger.gz
	SRR31174463_1.fastq.gz	Fastqsanger.gz

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Hexokinase 2 Exacerbates Mitochondrial Damage, Neuroinflammation, and Lipid accumulation by promoting ACSL4 ISGylation in Sepsis-Associated Encephalopathy

Project description:Metabolic reprogramming is often observed in sepsis-associated encephalopathy (SAE). However, little is known about the aberrant metabolic genes involved in mitochondrial damage, neuroinflammation, and lipid accumulation in microglial cells. Here, we show that hexokinase 2 (HK2) is upregulated and is strongly associated with the inflammatory response and lipid metabolism in lipopolysaccharide-induced BV2 cells. Genetic silencing or pharmacological inhibition of HK2 attenuates mitochondrial damage in vitro. Downregulation of HK2 lowered the NOD-like receptor signaling family pyrin domain containing three activations, both in BV2 cells and in the hippocampus of cecal ligation and puncture-induced male septic mice. Moreover, the inhibition of HK2 promoted lipid droplet reduction and activated mammalian target of rapamycin-mediated autophagy. Mechanistically, HK2 knockdown in microglial cells reduced the ISGylation of Acyl-CoA Synthetase Long-chain Family Member 4 (ACSL4) during lipid metabolism by interferon-stimulated gene 15 (ISG15). Notably, ISG15 eﬀectively down-regulated the expression of ACSL4 in vitro. Our findings provide new mechanistic insights of HK2 in microglial cells through regulation of ACSL4 ISGylation, suggesting a promising therapeutic strategy for treating SAE by targeting HK2.

2025-04-30 | GSE280721 | GEO

AS-exos exacerbates microglial ferroptosis-driven neuroinflammation

Project description:AS-exos exacerbates microglial ferroptosis-driven neuroinflammation

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RNA-seq data in cardiac tissues from cardiomyocyte-specific Acsl4 knockout mice after transverse aortic constriction

Project description:In order to investigate the differentially expressed genes in Acsl4 knockout after TAC (Transverse aortic constriction) or sham surgery. The experiment was divided to four groups including sham-operated Acsl4 flox/flox mice (FS), sham-operated Acsl4 knockout mice (KS), TAC-operated Acsl4 flox/flox mice (FT), TAC-operated Acsl4 knockout mice (KT) n=3 mice/group. The heart tissue was isolated after 21 days after performing TAC or sham surgery.

2024-08-26 | E-MTAB-14383 | biostudies-arrayexpress

The effect of ACSL4 expression on overall gene expression in breast cancer cell lines

Project description:ACSL4 expression appears to be inversely associated with steroid hormone and growth factor receptor expression in breast cancer and positively correlated with an aggressive breast cancer phenotype. Neither MCF-7 nor SKBr3 cells normally express ACSL4, and when manipulated to do so, develop basal-like characteristics, including increased proliferation, migration and anchorage independent growth. We used an Affymetrix array platform to assess changes in individual gene expression as a function of conditional and stable expression of ACSL4 in MCF-7 and SKBr3 cells. In experiment 1, MCF-7 Tet-ON cells were transfected with ACSL4 cDNA and induced to express ACSL4 by addition of 1ug/ml of doxycycline (A) or vehicle (C) for 72 hours. Three controls (C) and three doxycycline-induced (A) samples were evaluated for gene expression. In experiment 2, MCF-7 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A). In experiment 3, SKBr3 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A).

2012-09-19 | E-GEOD-40968 | biostudies-arrayexpress

Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

Project description:Background: Characterized by high incidence, mutilation, and death rate, acute ischemic stroke (AIS) has threatened people’s health seriously. Therefore, there is an urge need for early diagnosis and effective treatment of AIS. The purpose of this study was to clarify the regulatory role and potential molecular mechanism of miR-342-5p and circRNA_0008146 in AIS. Materials and Methods: Small RNA sequencing analysis was performed to screen differentially expressed miRNAs between the AIS and control group. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. The circRNA_0008146 and miRNA expression levels were detected by quantitative real-time PCR. Assay kits were used to determine Fe2+ levels and assess a battery of oxidative stress indicators, including ROS, MDA, LPO, SOD, and GSH/GSSG. The content of ACSL4 was measured by Western blot. The neurobehavioral manifestation was evaluated using the modified Neurological Severity (mNSS) Score, rotarod test, and corner test. TTC staining was employed to detect cerebral infarction volume. Nissl staining was adapted to detect histological change and neuronal damage. Results: RNA sequencing analysis revealed miR-342-5p was significantly downregulated in the plasma of AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic-reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. CircRNA_0008146 acted as a sponge of miR-342-5p, and overexpression of circRNA_0008146 increased brain damage in stroke mice. CircRNA_0008146 contributed to ferroptosis in cerebral infraction via sponging miR-342-5p to regulate ACSL4. Conclusion: CircRNA_0008146/miR-342-5p/ACSL4 axis regulate ferroptosis after cerebral ischemia-reperfusion, which may be a potential therapeutic target for ischemic stroke.

2024-08-08 | GSE254322 | GEO

ACSL4 effect on renal ischemia-reperfusion (I/R) injury

Project description:Analysis of acute kidney injury (AKI) with knockdown of ACSL4. Results provide insight into the role of ACSL4 in the regulation of ferroptosis.

2022-02-23 | GSE181842 | GEO

Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

Project description:Circ_0008146 exacerbates ferroptosis via regulating miR-342-5p/ACSL4 axis after cerebral ischemia-reperfusion in mice

| PRJNA1069739 | ENA

Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

Project description:Analysis of knockout ACSL4 gene in mouse colorectal cancer cell line. These results are for the role of the ACSL4 gene in colorectal cancer.

2024-12-31 | GSE283772 | GEO

hexokinase study

Project description:study of nucleotide sequence of hexokinase gene

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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer [T84 cells]

Project description:Analysis of ACSL4 gene knockout in human colorectal cancer cell line. These results confirm the role of the ACSL4 gene in colorectal cancer.

2024-12-31 | GSE284613 | GEO

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