Stress responsive gene FKBP5 mediates alcohol-induced liver injury through hippo pathway and CXCL1 signaling
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE155830 | GEO | 2023/07/23
REPOSITORIES: GEO
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Project description:Stress responsive gene FKBP5 mediates alcohol-induced liver injury through hippo pathway and CXCL1 signaling
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Project description:To further explore the overall development and progression of hepatic steatosis induced by HiAlc Kpn, we examined liver transcriptional profiles derived HiAlc Kpn-fed, pair-fed, or ethanol-fed mice for the 4th, 6th and 8th week post gavage. The liver gene expressions in mice both with HiAlc Kpn-fed and ethanol-fed have been showed large diversities to pair-fed mice. These results clearly illustrated a process of chronic liver injury, which is consistent with previous “two-hits” insulin hypothesis, and suggested that endogenous ethanol produced by HiAlc Kpn play important roles in the steatohepatitis, as well as alcohol intake.
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Project description:Consumption of ethanol has detrimental effects on gastric organs such as the intestine. To demonstrate the deleterious effect of alcohol, we sacrificed isobaric feeding or ethanol feeding mice and sorted the dendritic cells from their intestine organ. The dendritic cells were analyzed by a small-scale global proteomics approach. We achieved to obtain the biological signatures in the alcohol abuse mice group using bioinformatics analysis.
2024-06-16 | PXD033700 | Pride
Project description:Sprague-Dawley rats were placed on an ethanol-containing or pair-fed Lieber and DeCarli diets for 4 wks prior to surgical fracture. Following insertion of a medullary pin, a closed mid-diaphyseal fracture was induced using a Bonnarens and Einhorn fracture device. At 3 days post-fracture, the region of the fracture calluses were harvested from the right hind-limb. RNA was extracted and microarray analysis was conducted against the entire rat genome to study the effects of alcohol-consumption on the fracture healing. The experiments were on four rat subjects, i.e., pair-fed rats with subsequent surgical fracture or no surgical fracture, and alcohol-fed rats with subsequent surgical fracture or no surgical fracture. Each rat subject described above has three replicates so 6 kinds of pairing can be made and each pairing has a dye-swap replicate (thus, a total 12 array experiments). The focus of this study is on the pair-fed fracture subject vs. alcohol-fed fracture subject.
2011-05-01 | E-GEOD-16003 | biostudies-arrayexpress
Project description:FKBP5 is a long glucocorticoid-inducible gene implicated in psychiatric disorders. To investigate the complexities of chromatin interaction frequencies at the FKBP5 topologically associated domain (TAD), we deployed fifteen one-to-all chromatin capture viewpoints near gene promoters, enhancers, introns, and CTCF-loop anchors. This revealed a ‘one-TAD-one-gene’ structure encompassing the FKBP5 promoter and its enhancers. The FKBP5 promoter and its two glucocorticoid-stimulated enhancers roam the entire TAD while displaying subtle cell type-specific interactomes. The FKBP5 TAD consists of two nested CTCF loops that are coordinated by one CTCF site beyond the FKBP5 polyadenylation site and another in its 8th intron, 61 kb further. Loop extension correlates with transcription increases through the intronic CTCF site. This is efficiently compensated for, since the short loop is restored even under high transcription regimes. The boundaries of the FKBP5 TAD consist of divergent CTCF sites, harbor multiple smaller genes and are resilient to glucocorticoid stimulation. Interestingly, both FKBP5 TAD boundaries harbor H3K27me3-marked heterochromatin blocks that may reinforce them. We propose that cis-acting genetic and epigenetic polymorphisms underlying FKBP5 expression variation are likely to reside within a 240 kb region that consists of the FKBP5 TAD, its left sub-TAD, and both its boundaries.
2023-10-15 | GSE136034 | GEO
Project description:Sprague-Dawley rats were placed on an ethanol-containing or pair-fed Lieber and DeCarli diets for 4 wks prior to surgical fracture. Following insertion of a medullary pin, a closed mid-diaphyseal fracture was induced using a Bonnarens and Einhorn fracture device. At 3 days post-fracture, the region of the fracture calluses were harvested from the right hind-limb. RNA was extracted and microarray analysis was conducted against the entire rat genome to study the effects of alcohol-consumption on the fracture healing.
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Project description:Whole forestomach of mice treated with 20% ethanol for 4 weeks; Whole forestomach of mice treated with 15% ethanol for 40 weeks; negative control (0% alcohol treated mice)
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Project description:the molecular mechanisms for the biphasic effect of alcohol are not fully understood. The goal of the study is to identify genes that are differentially expressed following alcohol exposure of 50mM and 100mM ethanol for 24 hours.
2010-04-05 | GSE12253 | GEO
Project description:Breast cancer is the second leading cause of cancer-related deaths in women (*). Many genetic and behavioral risk factors can contribute to the initiation and progression of breast cancer, one being alcohol consumption. Numerous epidemiological studies have established a positive correlation between alcohol consumption and breast cancer; however, the molecular basis for this link remains ill defined. Elucidating ethanol-induced changes to global transcriptional programming in breast cells is important to ultimately understand how alcohol and breast cancer are connected mechanistically. We investigated early induced transcriptional changes in response to cellular exposure to moderate levels of alcohol. We treated the non-tumorigenic breast cell line MCF10A, and the tumorigenic breast cell lines MDA-MB-231 and MCF7, with ethanol for 6 h, then captured the changes to ongoing transcription using 4-thiouridine metabolic labeling followed by deep sequencing. Only the MCF10A cell line exhibited statistically significant changes to ongoing transcription in response to ethanol treatment. Further experiments revealed some ethanol-upregulated genes are sensitive to the dose of alcohol treatment, while others are not. Gene ontology and biochemical pathway analyses revealed that ethanol-upregulated genes in MCF10A cells are enriched in biological functions that could contribute to cancer development.
2023-08-04 | GSE221280 | GEO
Project description:Alcoholism is a complex disorder determined by interactions between genetic and environmental risk factors. Drosophila represents a powerful model system to dissect the genetic architecture of alcohol sensitivity, as large numbers of flies can readily be reared in defined genetic backgrounds and under controlled environmental conditions. Furthermore, flies exposed to ethanol undergo physiological and behavioral changes that resemble human alcohol intoxication, including loss of postural control, sedation, and development of tolerance. We performed artificial selection for alcohol sensitivity for 25 generations and created duplicate selection lines that are either highly sensitive or resistant to ethanol exposure along with unselected control lines. We used whole genome expression analysis to identify 1,678 probe sets with different expression levels between the divergent lines, pooled across replicates, at a false discovery rate of q < 0.001. We assessed to what extent genes with altered transcriptional regulation might be causally associated with ethanol sensitivity by measuring alcohol sensitivity of 37 co-isogenic P-element insertional mutations in 35 candidate genes, and found that 32 of these mutants differed in sensitivity to ethanol exposure from their co-isogenic controls. Furthermore, 23 of these novel genes have human orthologues. Combining whole genome expression profiling with selection for genetically divergent lines is an effective approach for identifying candidate genes that affect complex traits, such as alcohol sensitivity. Because of evolutionary conservation of function, it is likely that human orthologues of genes affecting alcohol sensitivity in Drosophila may contribute to alcohol-associated phenotypes in humans. Keywords: artificial selection, whole genome expression profiling
2007-11-20 | GSE7614 | GEO