Ontology highlight
ABSTRACT:
PROVIDER: PRJNA689632 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13358757_1.fastq.gz | Fastqsanger.gz | |||
| SRR13358757_2.fastq.gz | Fastqsanger.gz | |||
| SRR13358758_1.fastq.gz | Fastqsanger.gz | |||
| SRR13358758_2.fastq.gz | Fastqsanger.gz | |||
| SRR13358759_1.fastq.gz | Fastqsanger.gz |
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Project description:Unsaturated fatty acids (UFAs) in beef are essential for human health. Long-chain fatty acyl-CoA synthase 1 (ACSL1) is a crucial gene for UFAs synthesis in bovine adipocytes. To assess the protein expression profile during UFAs synthesis, we performed a proteomic analysis of bovine adipocytes by RNA interference and non-interference with ACSL1 using label-free techniques.
2024-03-15 | PXD050702 |
Project description:Systematic analyses of the temporal dynamics of transcriptomes and chromatin landscapes of macrophages during timecourse of TLR4-mediated inflammatory response. As a multifunctional effector cell, macrophages play pivotal roles in both the induction and resolution components of varied inflammatory processes. During the course of an inflammation response, macrophages engage in a homeostatic program characterized by tightly coordinated modulation of temporal outputs of both lipid metabolism and inflammation. We demonstrate inversely biphasic temporal dynamics of specific fatty acid metabolic and inflammatory gene expression profiles, associated with concordant temporal reprogramming of macrophage fatty acid profiles. In part, the late phase of the macrophage inflammatory response is characterized by tailoring of fatty acid related gene expressions, facilitating both significant induction of anti-inflammatory unsaturated fatty acid production and associated resolution of inflammation. We demonstrate the biphasic temporal dynamics of macrophage inflammation, specifically anti-inflammatory omega-3 and omega-9 unsaturated fatty acid levels, are transcriptionally driven genome-wide by an unexpected shift from an LXR to SREBP1-dominant regulatory program in the late phase inflammatory response. Collectively, our findings reveal a novel Srebp1-driven mechanism allowing the intimate inverse temporal relationship between the transcriptional regulation of inflammatory and fatty acid metabolic outputs; whereby modulation key transcriptional regulators (LXR, SREBP1 and NF-kB) of these pathways coordinate appropriate temporal tailoring of local enhancer associated reprogramming and eventual pathway regulatory interactions, during the course of TLR4-dependent inflammatory response in macrophages. This specific Srebp-driven, temporal reprogramming of macrophage fatty acid metabolism, characterized by late phase induction of anti-inflammatory unsaturated fatty acid production, is necessary for appropriate resolution of inflammation. Thus, this study suggests that selective reprogramming of macrophage lipid metabolism can serve as a viable therapeutic intervention aimed at ameliorating chronic inflammation and varied metabolic syndrome associated states.
2017-01-04 | GSE79423 | GEO
Project description:Diabetes mellitus is considered a relative contraindication for oral implant therapy, as hyperglycemia frequently precipitates vascular and osseous pathologies. Although clinicians routinely prioritize glycemic control before initiating implant-related treatment plans, diabetic patients often exhibit impaired osseointegration. However, the specific mechanisms remain to be elucidated. Emerging evidence suggests that this refractory bone loss is mediated by trained immunity, a process in which innate immune cells retain an epigenetic memory of prior inflammatory stimuli and mount an exaggerated response upon secondary challenge such as the invasive implantation process or inflammatory insult. Here, integrating RNA-seq, metabolomics, and ATAC-seq analyses, we demonstrate that stringent glycemic control in type I diabetes fails to normalize fatty-acid biosynthetic process, which remain persistently activated and potentiate macrophage-mediated inflammation and osteoclastogenesis when experiencing the secondary challenge. Mechanistically, prior hyperglycemic exposure enhances chromatin accessibility and sustaining Acsl1 transcription by H3K4me1 epigenetic modification at the Acsl1 locus in macrophages. This epigenetic imprint augments fatty-acid anabolism, amplifies pro-inflammatory cytokine production, and accelerates osteoclastic differentiation, ultimately compromising osseous repair. Collectively, our findings reveal that diabetes-induced H3K4me1 modification at Acsl1 drives metabolic reprogramming underpinning trained immunity and consequent bone damage. Targeting H3K4me1 or Acsl1 therefore represents a promising therapeutic strategy to improve implant osseointegration and skeletal regeneration in diabetic patients.
2026-02-05 | GSE318283 | GEO
Project description:Diabetes mellitus is considered a relative contraindication for oral implant therapy, as hyperglycemia frequently precipitates vascular and osseous pathologies. Although clinicians routinely prioritize glycemic control before initiating implant-related treatment plans, diabetic patients often exhibit impaired osseointegration. However, the specific mechanisms remain to be elucidated. Emerging evidence suggests that this refractory bone loss is mediated by trained immunity, a process in which innate immune cells retain an epigenetic memory of prior inflammatory stimuli and mount an exaggerated response upon secondary challenge such as the invasive implantation process or inflammatory insult. Here, integrating RNA-seq, metabolomics, and ATAC-seq analyses, we demonstrate that stringent glycemic control in type I diabetes fails to normalize fatty-acid biosynthetic process, which remain persistently activated and potentiate macrophage-mediated inflammation and osteoclastogenesis when experiencing the secondary challenge. Mechanistically, prior hyperglycemic exposure enhances chromatin accessibility and sustaining Acsl1 transcription by H3K4me1 epigenetic modification at the Acsl1 locus in macrophages. This epigenetic imprint augments fatty-acid anabolism, amplifies pro-inflammatory cytokine production, and accelerates osteoclastic differentiation, ultimately compromising osseous repair. Collectively, our findings reveal that diabetes-induced H3K4me1 modification at Acsl1 drives metabolic reprogramming underpinning trained immunity and consequent bone damage. Targeting H3K4me1 or Acsl1 therefore represents a promising therapeutic strategy to improve implant osseointegration and skeletal regeneration in diabetic patients.
2026-02-05 | GSE318284 | GEO
Project description:Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90% Two-condition experiment, cadiac gene expression of Acsl1H-/- vs Acsl1flox/flox mice 10 weeks after tamoxifen treatment. Biological replicates: 3-4 per condition.
2014-09-29 | E-GEOD-51913 | biostudies-arrayexpress
Project description:We applied single-cell ATAC sequencing and lipid profiling to inguinal and epididymal adipose depots from mice that received sham surgery or vertical sleeve gastrectomy (VSG). We observed depot-specific cellular composition and chromatin accessibility patterns that were altered by VSG. Specifically, accessibility at Scd1, a fatty acid desaturase, was substantially reduced after VSG in mature adipocytes of inguinal but not epididymal depots. This was accompanied by reduced accumulation of SCD1-produced unsaturated fatty acids. Given these findings and reports that reductions in Scd1 attenuate obesity and insulin resistance our results suggest VSG exerts its beneficial effects through an inguinal depot-specific reduction of SCD1 activity.
2021-12-20 | GSE191064 | GEO
Project description:Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90%
2014-09-29 | GSE51913 | GEO
Project description:NAT10 is an RNA cytidine transferase known to add acetyl group on RNA transcripts thereby promoting translational efficiency. It was reported that NAT10 regulates epithelial to mesenchymal transition (EMT), DNA damage, and cell proliferation in cancers. However, weather NAT10 regulates other crucial pathways is unknown. In our study we conducted gene expression profiling analysis using data obtained from RNA-seq of MCF7 NAT10 KO and scramble control. High throughput sequencing revealed fatty acid metabolism as the top enriched pathway with fatty acid metabolic genes such ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB, and ACAT1 were found to be differentially down-regulated. Overall our results revealed NAT10 depletion suppresses fatty acid metabolism in MCF7.
2022-08-03 | GSE210086 | GEO
Project description:The 21st century is an era of molecular breeding, leading to fundamental dairy market and production system changes. Milk fat is the main economic trait in dairy cattle production. Our previous study revealed that the ACADSB gene has a crucial regulatory role in lipid metabolism, which can alter the contents of TGs, CHOL and fatty acids by regulating some related gene which involve in lipid metabolism. As usual, when we explored the function of interest genes, we often design interference and overexpression vectors to regulate the expression level of related gene, and transiently transfect vectors into cells, however, it is limited by transfection efficiency. therefore, we committed to finding a stable mode of gene expression. Knocking out of the ACADSB gene in bovine mammalian epithelial cells (bMECs), which represents a promising and effective means of further research on the effects of ACADSB in vivo lipid metabolism of dairy cattle. At the same time, the knock-out ACADSB gene's bMECs could also be useful genetic material and tools for future research into gene functions related to lipid and fatty acid metabolism, which also can directly use for further exploring the gene molecular mechanism or related pathway.
2021-08-10 | GSE181131 | GEO