Comparative Effects of Arecoline, Caffeine, and Nicotine on Transcription Level in the NAc of Mice
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ABSTRACT:
PROVIDER: PRJNA1177499 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31110150_1.fastq.gz | Fastqsanger.gz | |||
| SRR31110150_2.fastq.gz | Fastqsanger.gz | |||
| SRR31110151_1.fastq.gz | Fastqsanger.gz | |||
| SRR31110151_2.fastq.gz | Fastqsanger.gz | |||
| SRR31110152_1.fastq.gz | Fastqsanger.gz |
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Project description:Though widely consumed, current research on the neural mechanisms of arecoline, caffeine, and nicotine remains limited, and the similarities and differences of these three substances on the nervous system are still not clear. This study used RNA-seq to analyze the gene expression in the nucleus accumbens (NAc) of mice, and further compared the behavioral changes through open field and conditioned place preference (CPP), exploring the effects of different psychoactive substances at the transcriptional and behavioral levels. Gene Ontology enrichment analysis revealed that nicotine and caffeine significantly alter biological processes related to synaptic function, and KEGG pathway analysis showed that the differentially expressed genes in the nicotine-treated group were significantly more enriched in pathways related to substance dependence compared to the other two treatment groups, with arecoline showing the least enrichment. Furthermore, only acute caffeine treatment significantly increased mouse activity, and only nicotine induced CPP. These results provided a scientific basis for evaluating the effects of arecoline, caffeine, and nicotine on the nervous system.
2024-11-11 | GSE280272 | GEO
Project description:Identify the methylation level of genes in epithelial cells stimulated with arecoline, a main component of betel quid.
2020-09-02 | GSE157246 | GEO
Project description:Sex differences in behaviors relevant to nicotine addiction have been observed in rodent models and human subjects. Behavioral, imaging and epidemiological studies also suggest underlying sex differences in mesolimbic dopamine signaling pathways. In this study we evaluated the proteome in the ventral tegmental area (VTA) and nucleus accumbens (NAc) shell in male and female mice. Experimental groups included two mouse strains (C3H/HeJ and C57BL/6J) at baseline, a sub-chronic, rewarding regimen of nicotine in C3H/HeJ mice, and chronic nicotine administration and withdrawal in C57BL/6J mice. Isobaric labeling with a TMT 10-plex system, sample fractionation, and tandem mass spectrometry were used to quantify changes in protein abundance. Similar or greater numbers of differentially regulated proteins were found between sexes at baseline in C3H/HeJ or C57BL/6J mice than within sexes following their respective regimen of nicotine administration. Despite differences by sex, strain, and nicotine exposure parameters, glial fibrillary acidic protein (GFAP) and dopamine and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32, Ppp1r1b) were repeatedly identified as significantly altered proteins, especially in the VTA. Further, network analyses showed sex- and nicotine-dependent regulation of a number of signaling pathways, including dopaminergic signaling. Sub-chronic nicotine exposure in female mice increased proteins related to dopaminergic signaling in the NAc shell but decreased them in the VTA, whereas the opposite pattern was observed in male mice. In contrast, dopaminergic signaling pathways were similarly upregulated in both male and female VTA after chronic nicotine and withdrawal. Overall, this study identifies significant sex differences in the proteome of the mesolimbic system, at baseline and after nicotine reward or withdrawal, which may help explain differential trajectories and susceptibility to nicotine addiction in males and females.
2021-06-28 | PXD023859 | Pride
Project description:To identify the presence of a novel gene in epithelial cells stimulated with arecoline, a main component of betel quid.
2020-09-02 | GSE157247 | GEO
Project description:Our previous research demonstrated that caffeine exposure on embryonic day (E) 8.5 increased body weight, altered cardiac morphology and function in adult male mice. However, these adverse effects were not observed in adenosine A1 receptor knockout (A1AR-/-) mice. Our hypothesis is that A1AR action mediates changes in DNA methylation patterns in mice exposed in utero to caffeine and that these changes in methylation lead to long-term effects in adult mice. To test this hypothesis, DNA Methylation 2.1M Deluxe Promoter Arrays (NimbleGen) were used to examine the methylation patterns of DNA isolated from adult left ventricles of the A1AR knockout line exposed to 20 mg/kg caffeine at E8.5 in utero. In A1AR+/+ mice, 4,896 hypermethylated and 2,823 hypomethylated regions were discovered in the left ventricles of the caffeine group compared to the normal saline group. In A1AR-/- mice, 1,024 hypermethylated and 1,757 hypomethylated regions were found in the caffeine group. The differentially methylated regions (DMRs) in the caffeine treated A1AR+/+ hearts mapped to 6,148 genes, 4,853 promoters, 4,111 primary transcripts, 816 CpG islands, and 98 miRNAs. Functional annotation clustering of genes revealed that many genes were involved in the development of hypertrophic cardiomyopathy and other heart diseases, which may explain our earlier findings of thickening of the left ventricular wall after in utero caffeine treatment. The methylation changes in several DMRs, mef2c, ins2, tnnt2, and myh6, were validated by bisulfite sequencing. In summary, in utero caffeine exposure caused DNA methylation changes in adult left ventricles and that these changes may be mediated by A1ARs. Pregnant mice were injected at embryonic day 8.5 with 0.9% NaCl (vehicle) or 20 mg/kg caffeine in vehicle i.p. Pups were born and raised until 8-10 weeks of age. Analysis was performed on the following groups vehicle A1AR+/+ (veh+/+), vehicle A1AR-/- (veh-/-), caffeine A1AR+/+ (caff+/+), and caffeine A1AR-/- (caff-/-). Genomic DNA from left ventricles of adult male mice was used. Two biological replicates were measured for each group.
2015-12-19 | E-GEOD-43030 | biostudies-arrayexpress
Project description:Background: Areca nut chewing is a major environmental risk factor for head and neck cancer (HNC), particularly in Southeast Asia. However, the molecular mechanisms that link areca nut exposure to malignant progression remain poorly understood. Long noncoding RNAs (lncRNAs) have emerged as critical regulators of oncogenesis, but their role in areca nut-associated HNC remains unexplored. Methods: We performed functional assays, transcriptomic profiling, and bioinformatic analyses to investigate the role of the lncRNA LUCAT1 in arecoline-treated HNC cells. Cell motility, epithelial–mesenchymal transition (EMT), reactive oxygen species (ROS) levels, and therapeutic resistance were assessed following LUCAT1 knockdown or overexpression. We identified upstream regulators of LUCAT1 through promoter analysis, transcription factor knockdown, and pharmacological inhibition. Results: LUCAT1 expression was significantly upregulated by arecoline exposure and promoted cell motility, EMT, ROS clearance, and resistance to radiotherapy and chemotherapy. Knockdown of LUCAT1 reversed these malignant phenotypes and suppressed antioxidant enzyme expression, partly through modulation of the p38 MAPK pathway. Transcriptomic and promoter analyses identified STAT1 as a key transcription factor activated by arecoline through muscarinic acetylcholine receptor (mAChR) signaling. Functional rescue experiments confirmed that LUCAT1 acts downstream of STAT1 to sustain arecoline-induced tumor aggressiveness. Conclusion: Our findings define a novel mAChR–STAT1–LUCAT1 regulatory axis that mediates areca nut-induced malignant progression in HNC. This study not only reveals a critical molecular pathway linking environmental carcinogen exposure to oncogenic transcriptional reprogramming but also highlights LUCAT1 as a promising target for therapeutic intervention in high-risk HNC patients.
2026-06-25 | GSE320559 | GEO
Project description:Caffeine is a globally consumed stimulant that has beneficial effects on biological processes including metabolism and aging, but its causal role in physiology remains incompletely understood. By using the roundworm Caenorhabditis elegans, here we show that caffeine extends lifespan by eliciting transcriptional remodeling that enhances lysosomal lipolysis. We found that transcriptomes of aged, caffeine-fed animals shifted toward youthful states. We also showed that caffeine induced a dietary restriction (DR)-like transcriptional program. Comparison with eat-2 mutants (a genetic DR model) identified commonly upregulated genes including the lysosomal lipases lipl-1 and lipl-2. The induction of lipl-1 and lipl-2 was required for increased lifespan and reduced neutral lipid accumulation by caffeine intake. Together, these findings indicate that caffeine promotes longevity in a DR-like metabolic reprogramming by enhancing lysosome-driven lipolysis.
2026-05-27 | GSE312248 | GEO
Project description:Genetic variants in gene regulatory sequences can modify gene expression and mediate the molecular response to environmental stimuli. In addition, genotype–environment interactions (GxE) contribute to complex traits such as cardiovascular disease. Caffeine is the most widely consumed stimulant and is known to produce a vascular response. To investigate GxE for caffeine, we treated vascular endothelial cells with caffeine and used a massively parallel reporter assay to measure allelic effects on gene regulation for over 43,000 genetic variants. We identified 665 variants with allelic effects on gene regulation and 6 variants that regulate the gene expression response to caffeine (GxE, false discovery rate [FDR] < 5%). When overlapping our GxE results with expression quantitative trait loci colocalized with coronary artery disease and hypertension, we dissected their regulatory mechanisms and showed a modulatory role for caffeine. Our results demonstrate that massively parallel reporter assay is a powerful approach to identify and molecularly characterize GxE in the specific context of caffeine consumption.
2024-02-26 | GSE221514 | GEO
Project description:To screen for xenobiotic-metabolizing-enzyme genes (XME) induced by caffeine exposure, a microarray experiment (performed with a Drosophila pangenomic array (Agilent 4 X 44K) was carried out between control and individuals exposed to caffeine (18mM ). Among 23401 genes consistantly found in the three biological replicates, 13108 showed a significant variation. 749 genes were over-expressed whereas 1518 were under-expressed. Interestingly, several genes belonging to all major classes of detoxification enzymes including XME were among the most highly induced such as CYP12d1, CYP6a8 and CYP6d5. Caffeine ingestion induced gene expression in Drosophila melanogaster male thorax and abdomen was mesured at 12h after exposure to doses of 0, 18mM of caffeine. Three independant experiments were performed at each dose using different drosophila for each experiment.
2014-07-04 | E-GEOD-59084 | biostudies-arrayexpress
Project description:Proteasomes hydrolyze most intracellular proteins. Immunoproteasome is a specific form of proteasome implicated in inflammation, cancer and autoimmune diseases. Modulation of immunoproteasome activity and content is a promising direction for the management of socially important pathologies. Using previously obtained reporter colorectal cancer cell lines, we tested how various commonly used compounds including ibuprofen, acetylsalicylic acid, vitamin C, caffeine and others, affect immunoproteasome expression. Methods: Immunoproteasome subunit expression was assessed by flow cytometry, qPCR and Western blot. Proteasome activity was tested using fluorogenic substrates and the activity probe. Transcriptome analysis was performed to identify patterns of gene expression changes. Results: Among the tested compounds caffeine was the only drug that revealed modest reduction in quantity of immunoproteasomes. The effect of caffeine on immunoproteasomes varied between cell lines and was stronger as a result of prolonged treatment. The reduction of immunoproteasome content in cells treated with caffeine coincided with decreased expression of immunoproteasome subunits and downregulation of Nrf3 transcription factor and a PAC4 proteasome assembly chaperone. Moreover, decreased expression of immunoproteasome subunits in cells treated with caffeine coincided with the reduction of oxidative stress levels. Caffeine did not affect the degradation of immunoproteasomes by autophagy. Conclusions: Modulation of immunoproteasome expression by caffeine might help to optimize existing and develop novel strategies for the treatment of colorectal cancer and several autoimmune diseases.
2024-10-22 | GSE279800 | GEO