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Non-coding small RNA expression analysis of rat pancreatic acinar cells(AR42J) treated with sodium taurocholate

ABSTRACT: Non-coding small RNA expression analysis of rat pancreatic acinar cells(AR42J) treated with sodium taurocholate

PROVIDER: PRJNA750677 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15295250.fastq.gz	Fastqsanger.gz
	SRR15295251.fastq.gz	Fastqsanger.gz
	SRR15295252.fastq.gz	Fastqsanger.gz
	SRR15295253.fastq.gz	Fastqsanger.gz
	SRR15295254.fastq.gz	Fastqsanger.gz

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Similar Datasets

Non-coding small RNA expression analysis of rat pancreatic acinar cells(AR42J) treated with sodium taurocholate

Project description:Acute pancreatitis (AP) is a common digestive disorder with high morbidity and mortality. At present, the pathogenic mechanisms of AP remain unclear. Pancreatic acinar intracellular trypsinogen activation is considered to be an important cause of AP and is an important event in the early stages of AP. The activation of trypsinogen is a key factor for the pancreas to maintain normal function and that the abnormal activation of trypsinogen in pancreatic acinar cells is an initiating factor for the occurrence of AP. In the past decade, microRNA-related research results suggest that small non-coding RNAs play an important role in AP. Recently, endogenous transfer RNA-derived small RNA (tsRNA), a newly identified non-coding small RNA, is reported to be associated with multiple diseases. tsRNAs can be broadly classified into two main groups: tiRNAs (tRNA halves) and tRFs (tRNA-derived fragments). tiRNAs are produced by specific cleavage in the anticodon loop under various stress conditions (29-50 nucleotides). tRFs are separated to 4 subtypes by their sites of origin in pre-tRNA or mature tRNA, and generally shorter than tiRNAs (16-28 nucleotides). Similar to the function of microRNA, tsRNA can inhibit their functions by binding to target genes. However, the role of tsRNA in regulating AP pathogenesis has not been investigated. In this experiment, sodium taurocholate was used to treat the rat pancreatic acinar cell (AR42J) to establish the AP-related intracellular activation of trypsinogen model. Then we used RNA sequencing to identify the differentially expressed non-coding small RNAs including microRNA and tsRNA in the cell model.

2023-09-17 | GSE181092 | GEO

Sodium taurocholate co-transporting polypeptide deficiency attenuates hepatocarcinogenesis in mice

Project description:Sodium taurocholate co-transporting polypeptide deficiency attenuates hepatocarcinogenesis in mice

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Zonation of pancreatic acinar cells in diabetic mice

Project description:We sequenced AR42J cell exposed to CCK or insulin in different concentrations. This enable us to uncover the possible effect of the different hormones on acinar cells in pathlogy.

2020-07-17 | GSE154533 | GEO

Sodium taurocholate co-transporting polypeptide deficiency attenuates hepatocarcinogenesis in mice

Project description:Sodium taurocholate co-transporting polypeptide (NTCP) is a liver specific bile acid (BA) transporter; this transporter also serves as a functional receptor for hepatitis B virus (HBV) and hepatitis D virus (HDV). Here, we generated mouse models to investigate the role of NTCP in hepatocarcinogenesis. We report that NTCP-deficient (Slc10a1-/-) mice with long-term hypercholanemia do not develop spontaneous hepatocellular carcinoma (HCC). Using a diethylnitrosamine (DEN)-induced mouse model of HCC, we found that Slc10a1-/- mice exhibited fewer liver tumors, while transgenic mice constitutively overexpressing mouse NTCP in hepatocytes Tg(mNTCP-C9) experienced increased tumor burdens. Intriguingly, the subset of male Slc10a1-/- mice with hypercholanemia exhibited a hepatic female-biased gene expression. Importantly, a majority of the human homologs of genes with significantly hepatic female-biased expression were found to be correlated with improved prognosis in human patients with liver cancer. Our ﬁndings indicate that pharmacological manipulation of NTCP function can have a clinical impact on decreasing risk of development or decreasing risk of death liver cancer.

2025-08-01 | GSE155870 | GEO

Increased sulfation of bile acids in mice and human subjects with sodium taurocholate cotransporting polypeptide deficiency

Project description:Increased sulfation of bile acids in mice and human subjects with sodium taurocholate cotransporting polypeptide deficiency

| PRJNA510995 | ENA

Increased sulfation of bile acids in mice and human subjects with sodium taurocholate cotransporting polypeptide deficiency

Project description:Purpose: To decipher the biochemical basis for the declining of total bile acids (TBA) levels in the late age of Slc10a1-/- mice, we performed a serial liver RNA-Seq analysis of mRNA expression with male mice at different ages. Methods: Liver mRNA profiles of 4-week, 8-week, 20-month-old wild-type (WT) and sodium taurocholate cotransporting polypeptide knockout (Slc10a1-/-) mice were generated by deep sequencing, in triplicate, quadruplicate or sextuplicate, using Illumina Hiseq-2500 platform. Clean mRNA-seq reads were aligned to the mouse reference genome (GRCm38) with TopHat (v2.0.13), guided by Ensembl gene annotation v83. Only uniquely aligned and properly paired reads were retained for further analysis. Gene-level read counts were calculated with HTseq (v0.6.1p1) with the union mode. Genes with less than a total of 11 non-normalized reads across all samples were excluded. Data normalization and statistical analysis of differential expression were performed with the DEseq2 (v1.10.0) R package. Pair-wise Spearman correlation between samples across all quantified genes used for hierarchical clustering. Results: At 4 weeks and 8 weeks, WT and Slc10a1-/- mice exhibited clear different pattern in terms of transcriptome similarity and were well separated, however, the difference was indistinguishable at 20 months.And changes of pathways involved in the metabolism of xenobiotics in Slc10a1-/- mice. Conclusions: Our study reveal that enhanced BA sulfation is a major mechanism for BA detoxification and elimination in Slc10a1-/- mice with hypercholanemia.

2019-06-13 | GSE124214 | GEO

Response of Candida albicans to taurocholate

Project description:Presence of taurocholate (TC), a constituent of bile, confers resistance of Candida albicans to antifungals like Caspofungin and Amphotericin B. Transcriptional profiles in presence and absence of TC were compared to determine whether an upregulation of known resistance genes is responsible for this effect. No upregulation was found, and the resistance seemed to be rather based on a direct interaction of TC with the antifungals.

2017-02-15 | E-MTAB-5277 | biostudies-arrayexpress

Effect of Sodium Valproate on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with sodium valproate treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses (500 uM and 10 mM) of sodium valproate and water vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis.

2012-08-28 | GSE40338 | GEO

RNA-Seq of explanted murine pancreatic acinar cells

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia, pancreatic acinar cells were isolated from 5 week old KrasG12D-mice. RNA was isolated immediately after isolation (t=0 days) or after 3 days embedded in collagen.

2023-03-02 | E-MTAB-9878 | biostudies-arrayexpress

A modular analysis reveals that kinase-associated gene groups are involved in taurolithocholic acid 3-sulfate (TLC-S)-induced biological processes of AR42J cells

Project description:Background: Bile acids can act on pancreatic acinar cells and induce intracellular trypsinogen activation, but the underlying molecular mechanism remains unknown.The present study aimed to investigate taurolithocholic acid 3-sulfate (TLC-S)-induced alterations of gene groups in AR42J cells using a modular analysis.Methods: After the pancreatic acinar AR42J cells were stimulated by TLC-S for 20 min, gene chip technology was applied to identify genes that were differentially expressed. Subsequently, the regulatory sub-networks of genetic interactions among the differentially expressed genes were constructed using the protein–protein interaction (PPI) network. Finally, the CFinder software was utilized to generate genetic modules, which were then subjected to a functional enrichment analysis.Results: The gene chip assay demonstrated that the expression levels of 1124 genes were upregulated and that those of 498 genes were downregulated in the TLC-S

2014-12-09 | GSE63959 | GEO

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