Ontology highlight
ABSTRACT:
PROVIDER: PRJNA810762 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18156076_1.fastq.gz | Fastqsanger.gz | |||
| SRR18156076_2.fastq.gz | Fastqsanger.gz | |||
| SRR18156077_1.fastq.gz | Fastqsanger.gz | |||
| SRR18156077_2.fastq.gz | Fastqsanger.gz | |||
| SRR18156078_1.fastq.gz | Fastqsanger.gz |
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Project description:Cardiac proteome analysis of obese rats treated with mitoQ
2023-06-29 | PXD034955 | JPOST Repository
Project description:In the current study, we investigated the modulatory effect of epigallocatechin gallate (EGCG, an active derivative of green tea) on cellular miRNA expression and cell cycle proliferation in NSCLCs (A549). As the IC50 value of EGCG is approximately 304 μM, our studies support the resistance of A549 lung cancer cell by EGCG. In addition, it was interesting to observe its G0/G1 cell cycle arrest activity at 40μM EGCG treatment. So, in the present study, next-generation sequencing (NGS) was used to study the miRNA expression between the cancer control and EGCG-treated samples. A549 cells were treated with 40 μM and 100 μM EGCG. NGS was employed to study the differential expression of novel and known miRNAs. The data generated was analysed with computational approach to study and correlate the expression profiles of both known and novel miRNAs. Differential expression of known miRNAs was observed between control and EGCG-treated samples. Some putative novel miRNA sequences were also observed in the current study. The differential expression levels of putative novel miRNA sequences were estimated by counting the number of reads in the given dataset. Together the analysis of these miRNA profiles revealed log2-fold modulation in the expression levels. We detected 344, 337, and 346 number of known mature miRNAs in control, 40 μM EGCG treated, and 100 μM EGCG treated samples, respectively. We also reported 119, 126, and 125 number of putative novel mature miRNA sequences in control, 40 μM EGCG treated, and 100 μM EGCG treated samples, respectively. In conclusion, the analysis demonstrates that EGCG is actively involved in miRNA modulation in NSCLCs, which further attests to its chemoprotective role and could play a major role in therapeutic applications.
2019-02-07 | GSE110514 | GEO
Project description:Background: Hepatocellular carcinoma (HCC) is increasing in incidence and treatment is often unsuccessful. Thus, prevention in high-risk patients with established cirrhosis has been proposed as an alternative strategy. It has been suggested that the increased inflammation and fibrogenesis observed during cirrhosis predisposes the liver to future malignant transformation to HCC through a “field effect”. A growing body of evidence indicates that the green tea polyphenol, (-)-epigallocatechin gallate (EGCG), can reduce inflammation and fibrogenesis during chronic liver injury. Here, we test the hypothesis that EGCG administered in the setting of cirrhosis can prevent future HCC development. Methods: A rat model of diethylnitrosamine (DEN)-induced cirrhosis was used to examine the efficacy of EGCG for inhibition of HCC formation in these cirrhotic livers. DEN (50 mg/kg) was administered weekly throughout the study while 0.02% EGCG was given in drinking water beginning at the onset of cirrhosis. At the end of the study, rats were sacrificed, livers were sectioned and stained to analyze disease progression and tumor nodules were counted. Liver function tests were performed to determine liver injury and overall liver function. Finally, genome-wide gene expression profiling on the surrounding, non-tumoral liver tissue was used to monitor the “field effect” in response to EGCG. Results: EGCG significantly (p < 0.01) prevented the development of HCC tumor nodules from on average 18.8 in vehicle controls to on average 9.1 in EGCG-treated animals. EGCG also reduced liver injury and improved liver function as assessed by serum chemistry tests. Finally, a gene expression signature predictive of poor survival and HCC development in human cirrhosis patients was reversed in response to EGCG. Conclusions: Our data are consistent with the growing body of evidence suggesting that EGCG has protective effects in liver disease. Further, our results suggest that EGCG is a potentially effective HCC prevention strategy that can be monitored using gene expression signatures.
2020-03-10 | GSE67880 | GEO
Project description:Mechanism (s) of the epigallocatechin-3-gallate (EGCG) as major effective components in green tea regarding the reduction of hypertensive risk might associate with microRNAs (miRNAs). The plasma distribution of EGCG and epigallocatechin (EGC) in Sprague-Dawley rats were analyzed pharmacokinetically and found that they did not distribute well in plasma but widely in tissues, and their plasma deposition best fitted a mono-compartmental model with Cmax (6.65 vs 4.45 μg/mL) and Tmax (15 vs 10 min). Blood pressure monitoring of spontaneously hypertensive rats (SHR) intragastrically administrated with 300 mg/kg BW showed that systolic blood pressure (SBP) decreased to the lowest point by 34.04 mmHg and recovered by 23.39 mmHg after 15 and 30 min of administration, respectively, and it decreased again at 60 min and recovered at time 2 h. Total 150 upregulated and 18 downregulated miRNAs were identified via the deep sequencing and were 1.0 or 0.5 fold to the control group (P<0.01) after EGCG administration. And, hypertension-associated miRNA-126-3p and miRNA-150 were further validated by qRT-PCR. It might help explore novel pathways involving antihypertensive effect of EGCG.
2018-01-20 | GSE109412 | GEO
Project description:We have identified Epigallocatechin Gallate (EGCG) as a potent modulator of microglia function. Our aim was to determine whether EGCG affects the transcriptome of microglia and identify genes and gene sets that may underly the effects of EGCG on microglia function.
2024-07-17 | GSE208144 | GEO
Project description:Diabetic rats changes gene exprssion in liraglutide treated rats cardiac muscle
2018-03-28 | GSE102194 | GEO
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days.
2011-02-11 | GSE21329 | GEO
Project description:Epigallocatechin-3-gallate (EGCG), a major active polyphenol of green tea, has been shown to downregulate inflammatory responses in macrophages; however, the underlying mechanism has not been understood. Recently, we identified the 67-kDa laminin receptor (67LR) as a cell-surface EGCG receptor that mediates the anti-cancer action of EGCG at physiologically relevant concentrations (0.1-1 mM). Here we show the molecular basis for the downregulation of TLR4 signal transduction by EGCG at 1 mM in macrophages. Anti-67LR antibody treatment or RNAi-mediated silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on LPS-induced activation of downstream signaling pathways and target gene expressions. Additionally, we found that EGCG reduced the TLR4 expression through 67LR. Interestingly, EGCG induced a rapid upregulation of Tollip protein, a negative regulator of TLR-signaling, and this EGCG action was prevented by 67LR silencing or anti-67LR antibody treatment. RNAi-mediated silencing of Tollip impaired the TLR4 signaling inhibitory activity of EGCG. Taken together, these findings demonstrate that 67LR plays a critical role in mediating anti-inflammatory action of a physiologically relevant EGCG and Tollip expression could be modulated through 67LR. These results provide a new insight into the understanding of negative regulatory mechanisms for TLR4 signaling pathway and consequent inflammatory responses which are implicated in the development and progression of many chronic diseases. We quantified expression profile of 210 inflammatory-relating genes in the 67LR-downregulated cells treated with LPS or/and EGCG by microarray
2010-04-20 | E-GEOD-21320 | biostudies-arrayexpress
Project description:We characterized the insulin sensitivity and multi-tissue gene expression profiles of lean and insulin resistant, obese Zucker rats untreated or treated with one of four PPARγ ligands (pioglitazone, rosiglitazone, troglitazone, and AG035029). We analyzed the transcriptional profiles of adipose tissue, skeletal muscle, and liver from the rats and determined whether ligand insulin-sensitizing potency was related to ligand-induced alteration of functional pathways. Ligand treatments improved insulin sensitivity in obese rats, albeit to varying degrees. Male Zucker fatty (fa/fa) and lean (fa/+) rats (Charles River, Wilmington, MA) were received at 6 weeks of age. Fatty rats were weight-matched upon arrival and randomly divided into one of five experimental groups. The fatty rat groups varied by the type of chow they were fed - normal chow alone or with a PPARγ ligand admixture: normal chow (fatty control, FC), rosiglitazone-treated (Rosi), pioglitazone-treated (Pio), troglitazone-treated (Tro), or AG035029-treated (AG). Lean control (LC) rats were all fed normal chow. Rats groups were maintained on the diets for 21 days. Adipose tissue (epididymal), skeletal muscle (gastrocnemius), and liver were harvested from lean (LC) and insulin resistant, obese Zucker rats untreated (FC) or treated with one of four PPARγ ligands (pioglitazone [Pio], rosiglitazone [Rosi], troglitazone [Tro], and AG035029 [AG]).
2011-02-11 | E-GEOD-21329 | biostudies-arrayexpress
Project description:Epigallocatechin-3-gallate (EGCG), a polyphenol, influences cutaneous wound healing due to its anti-angiogenic, anti-inflammatory and anti-oxidant properties. We previously demonstrated the role of EGCG in scarring in ex vivo human scar models. A double-blind randomised-controlled trial. Here, we evaluated application of topical EGCG compared with placebo in 62 healthy human volunteers, over 8 weeks, in scars created in their upper inner arms using skin punch biopsies. RNA sequencing was used here based on 45 samples: day 0 (n=3), week 1 (n=3 placebo, n=3 EGCG), week 2 (n=3 placebo, n=3 EGCG), week 3 (n=3 placebo, n=3 EGCG), week 4 (n=3 placebo, n=3 EGCG), week 5 (n=3 placebo, n=3 EGCG), week 6 (n=3 placebo, n=3 EGCG), week 8 (n=3 placebo, n=3 EGCG). The common differentially expressed genes identified between treated (EGCG) and placebo samples were grouped according to time point (Zonal priming: weeks 1 and 2; Direct application post scar formation (2 weeks post-biopsies): weeks 1, 2, 3, 4, 6). Further exploration of these genes using Gene Ontology and Ingenuity Pathway Analysis revealed gene signatures of relevant biological processes and pathways. Here, RNA sequencing revealed a number of angiogenic, inflammatory and antioxidant genes that were significantly downregulated with EGCG particularly at week 1 including; TPSAB1, VEGFA, EDF, IL17F, IL1A, IL1RL1, IL36A, IL36G, SOD3.
2019-05-01 | GSE124161 | GEO