Identification of significantly differential expression of long noncoding RNAs and pathways in hepatic fibrosis rat liver issues
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ABSTRACT:
PROVIDER: PRJNA723768 | ENA |
REPOSITORIES: ENA
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Project description:Objective: To identify the long noncoding (lncRNA) and its potential roles in hepatic fibrosis rat liver issues induced by CCl4. Methods: LncRNAs and genes were analyzed in fibrosis rat liver issues by RNA sequencing and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Differential expressed lncRNAs and genes were subjected to bioinformatics analysis and involved to construct co-expression network.
2021-04-23 | GSE173085 | GEO
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2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
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Project description:A differential label-fee proteomics approach was performed using 27 biopsies from patients with HCV-associated hepatic fibrosis. For statistical analysis the patients were grouped into a low and a high fibrosis group. The low fibrosis group contained 13 patients of fibrosis stages 0, 1 and 2, whereas the high fibrosis group contained 14 patients of fibrosis stages 3 and 4 (fibrosis stages according to Batts-Ludwig classification).
2015-03-30 | PXD001474 | Pride
Project description: Not available
| S-EPMC8486097 | biostudies-literature
Project description:Hepatic fibrosis, a common pathological manifestation of chronic liver injury, is generally considered to be the end result of an increase in extracellular matrix produced by activated hepatic stellate cells (HSCs). Targeting the mechanisms underlying HSC activation may provide a powerful therapeutic strategy for the prevention and treatment of liver fibrosis. A high-throughput screening assay was established, and the histone deacetylase inhibitor givinostat was identified as a potent inhibitor of HSC activation in vitro. Givinostat significantly inhibited HSC activation in vivo, ameliorated carbon tetrachloride-induced mouse liver fibrosis and lowered plasma aminotransferases. Transcriptomic analysis revealed the most significantly regulated genes in the givinostat treatment group in comparison with those in the solvent group, among which, Dmkn, Msln and Upk3b were identified as potential regulators of HSC activation. Givinostat significantly reduced the mRNA expression of Dmkn, Msln and Upk3b in both a mouse liver fibrosis model and in HSC-LX2 cells. Knocking down any of the aforementioned genes inhibited the TGF-β1-induced expression of α-smooth muscle actin and collagen type I, indicating that they are crucial for HSC activation. In summary, using a novel strategy targeting HSC activation, the present study identified a potential epigenetic drug for the treatment of hepatic fibrosis and revealed novel regulators of HSC activation.
2020-12-01 | GSE161981 | GEO
Project description:<p>Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important.</p><p><br></p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p>
2023-03-17 | MTBLS6732 | MetaboLights
Project description:<p>Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important.</p><p><br></p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p>
2023-03-17 | MTBLS6742 | MetaboLights
Project description:This study aimed to investigate the effects and underlying mechanisms of tormentic acid (TA) on carbon tetrachloride (CCl4)-induced liver fibrosis in rats. The rats were intragastrically administered with 50% CCl4 for 9 weeks to induce hepatic fibrosis, followed by various agents for 6 weeks. Transcriptomic analysis was carried out to predict the potential targets, and then multiple examinations were performed to verify the prediction. The results showed that TA significantly alleviated liver injury and fibrosis, as evidenced by the ameliorative pathological tissue, low transaminase activity, and decreased collagen accumulation. Besides, TA markedly reduced hepatocyte apoptosis by regulating the expression of caspase-3 and Bcl-2 families. The transcriptomic analysis revealed 2,173 differentially expressed genes (DEGs) between the TA and model groups, which could be enriched in the metabolic pathways and the PI3K/Akt and NF-κB signaling pathways. The metabolomics analysis showed that TA could regulate the glycerophospholipid metabolism pathway by regulating the synthesis of phosphatidylserines, phosphatidylethanolamines and phosphatidylcholines. Moreover, the integrative analysis of the transcriptomics and metabolomics data indicated that TA inhibited the glycerophospholipid metabolism pathway by inhibiting the expression of LPCAT4, PTDSS2, PLA2G2A and CEPT1. In addition, the relevant signaling pathways analysis confirmed that TA inhibited HSCs activation by blocking the PI3K/Akt/mTOR pathway and ameliorated inflammatory injury by inhibiting the NF-κB pathway. In conclusion, TA significantly alleviates liver fibrosis in vivo by inhibiting the glycerophospholipid metabolism pathway and the PI3K/Akt/mTOR and NF-κB signaling pathways.
2021-11-13 | GSE188604 | GEO
Project description:<p><em>Parabacteroides distasonis</em> (<em>P. distasonis</em>) plays an important role in human health, including diabetes, colorectal cancer and inflammatory bowel disease. Here, we show that <em>P. distasonis</em> is decreased in patients with hepatic fibrosis, and that administration of P. distasonis to mice improves thioacetamide (TAA)- and methionine and choline deficient (MCD) diet-induced hepatic fibrosis. <em>P. distasonis</em> was associated with increased bile salt hydrolase (BSH) activity and inhibition of intestinal farnesoid X receptor (FXR) signaling leading to decreased taurochenodeoxycholic acid (TCDCA) levels in liver. The decrease of TCDCA improved activation of hepatic stellate cells (HSCs) through decreasing the mitochondrial permeability transition (MPT)-Caspase-11 pyroptosis pathway. Celastrol was demonstrated as a promoter of <em>P. distasonis</em>, which could inhibit intestinal FXR and increase the excretion of bile acids, leading to decreased hepatic TCDCA and prevention against TAA- and MCD diet-induced hepatic fibrosis. These data suggest that supplementation of <em>P. distasonis</em> may be a promising means to ameliorate hepatic fibrosis.</p><p><br></p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p>
2023-03-17 | MTBLS6728 | MetaboLights
Project description:Liver fibrosis is a strong predictor of long-term mortality in patients with non-alcoholic fatty liver disease; yet the mechanisms underlying the progression from the comparatively benign fatty liver state to advanced non-alcoholic steatohepatitis (NASH) and liver fibrosis are incompletely under-stood. Using a cell type-resolved genomics approach, we show that comprehensive alterations in hepatocyte genomic and transcriptional settings during NASH progression, led to a partial loss of hepatocyte identity. The hepatocyte reprogramming was under tight cooperative control of a net-work of NASH-activated transcription factors (TFs), as exemplified by Elf3 and Glis2. Indeed, Elf3 and Glis2 controlled hepatocyte identity and fibrosis-dependent hepatokine genes targeting disease-associated hepatic stellate cell (HSC) gene programs. Thus, interconnected TF networks not only promoted hepatocyte dysfunction, but also directed the intra-hepatic crosstalk with HSCs necessary for NASH and fibrosis progression implying molecular “hub-centered” targeting strategies to be superior to existing mono-target approaches as currently used in NASH therapy.
2021-07-13 | PXD025691 | Pride