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Bulk RNA sequencing on hepatic tissues from colitis mice treated with a sublethal indirubin dose.

ABSTRACT: Bulk RNA sequencing on hepatic tissues from colitis mice treated with a sublethal indirubin dose.

PROVIDER: PRJNA1276473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33979164_1.fastq.gz	Fastqsanger.gz
	SRR33979164_2.fastq.gz	Fastqsanger.gz
	SRR33979165_1.fastq.gz	Fastqsanger.gz
	SRR33979165_2.fastq.gz	Fastqsanger.gz
	SRR33979166_1.fastq.gz	Fastqsanger.gz

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Bulk RNA sequencing on hepatic tissues from colitis mice treated with a sublethal indirubin dose.

Project description:Many plant-derived bioactive molecules with low solubility and permeability can cause hepatocyte injury. However, the mechanism by which they induce hepatic damage without passive diffusion into the hepatic circulatory system remains unclear. In this study, we demonstrate that indirubin, the main component of indigo naturalis with poor aqueous solubility, predisposes mice with chronic colitis to hepatic injury. This closely mimics the hepatic damage commonly observed in ulcerative colitis patients treated with indigo naturalis. To elucidate the mechanism of indirubin-induced hepatocyte injury in chronic colitis, we performed bulk RNA sequencing on hepatic tissues from DSS-induced colitis mice treated with a sublethal indirubin dose.

2025-06-15 | GSE299769 | GEO

Treatment of Candida albicans with sublethal concentration of keanumycin A

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Dose-dependent metabolic reprogramming and differential gene expression in TCDD-elicited hepatic fibrosis

Project description:We have previously shown that in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-elicited NAFLD progression, central carbon, glutaminolysis and serine/folate metabolism are reprogrammed to support NADPH production and ROS defenses. To further investigate underlying dose-dependent responses associated with TCDD-induced fibrosis, female C57BL/6 mice were gavaged with TCDD every 4 days (d) for 28d or 92d. RNA-Seq, ChIP-Seq (2hr), and 28d metabolomic (urine, serum, and hepatic extract) analyses were conducted with complementary serum marker assessments at 92d. Additional vehicle and 30 µg/kg treatment groups were allowed to recover for 36d following the 92d treatment regimen to examine recovery from TCDD-elicited fibrosis. Histopathology revealed dose-dependent increases in hepatic fat accumulation, inflammation, and periportal collagen deposition at 92d, with increased fibrotic severity in the recovery group. Serum proinflammatory and profibrotic interleukins-1β, -2, -4, -6, and -10, as well as TNFα and IFNγ, exhibited dose-dependent induction. An increase in glucose tolerance was observed with a concomitant 3.0-fold decrease in hepatic glycogen linked to increased ascorbic acid biosynthesis and proline metabolism, consistent with increased fibrosis. RNA-Seq identified differential expression of numerous matrisome genes including an 8.8-fold increase in Tgfb2 indicating myofibroblast activation. Further analysis suggests reprogramming of glycogen, ascorbic acid, and amino acid metabolism in support of collagen deposition and the use of proline as a substrate for ATP production via the proline cycle. Conclusion: In addition to metabolic reprogramming in support of NADPH production for ROS defense, we demonstrate that glycogen, ascorbic acid, and amino acid metabolism are also reorganized to support remodeling of the extracellular matrix, progressing to hepatic fibrosis in response to chronic injury from TCDD.

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RNA-Seq Analysis of Dose-Dependent TCDD-Elicited Hepatic Gene Expression in Male Mice

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Dose-dependent hepatic transcriptional responses in Atlantic salmon (Salmo salar) exposed to sublethal doses of gamma radiation

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Stress response in Escherichia coli following sublethal phenalene-1-one mediated antimicrobial photodynamic therapy: an RNA-Seq study

Project description:Since the molecular mechanisms behind adaptation and the bacterial stress response toward antimicrobial photodynamic therapy (aPDT) are not entirely clear yet, the aim of the present study was to investigate the transcriptomic stress response in Escherichia coli after sublethal treatment with aPDT using RNA sequencing (RNA-Seq). Planktonic cultures of stationary phase E. coli were treated with aPDT using a sublethal dose of the photosensitizer SAPYR. After treatment, RNA was extracted, and RNA-Seq was performed on the Illumina NextSeq 500. Differentially expressed genes were analyzed and validated by qRT-PCR. The analysis of the differential gene expression following pathway enrichment analysis revealed a considerable number of genes and pathways significantly up- or down-regulated in E. coli after sublethal treatment with aPDT. Expression of 1018 genes was up-regulated and of 648 genes was down-regulated after sublethal treatment with aPDT as compared to irradiated controls. Analysis of differentially expressed genes and significantly de-regulated pathways showed regulation of genes involved in oxidative stress response and bacterial membrane damage. In conclusion, the results show a transcriptomic stress response in E. coli upon exposure to aPDT using SAPYR and give an insight into potential molecular mechanisms that may result in development of adaptation

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RNA-Seq Versus Oligonucleotide Array Assessment of Dose-Dependent TCDD-elicited Hepatic Gene Expression in Mice [Array]

Project description:Dose-dependent hepatic gene expression was examined following repeated exposure (every 4 days for 28 days) to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). These data were used to examine the effect of repeated TCDD exposure as well as compare the performance of RNA-Seq and Agilent oligonucleotide microarrays for detection and identificatioin of differentially expressed genes. Three biological replicates for each dose (0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30) of TCDD and sesame oil vehicle This submission represents the Agilent microarrays component of study.

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