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Gene expression changes in rat lung induced by six pyrrolizidine alkaloids

ABSTRACT: Gene expression changes in rat lung induced by six pyrrolizidine alkaloids

PROVIDER: PRJNA699571 | ENA |

REPOSITORIES: ENA

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Gene expression changes in rat lung induced by six pyrrolizidine alkaloids

Project description:Pyrrolizidine alkaloids (PAs) are secondary plant metabolites that can be found worldwide. They can have an impact to human health by inducing acute toxic effects like veno-occlusive disease in the liver and pulmonary arterial hypertension in the lung. The study focuses on the identification of gene expression changes in vivo in rat lungs after treatment with six structurally different PAs (echimidine, heliotrine, lasiocarpine, senecionine, senkirkine or platyphylline). Rats were treated by gavage daily with 3.3 mg/kg body weight PAs for 28 days. After this subacute exposure the transcriptional changes in the lung were investigated by whole genome microarray analysis. Transcriptomic analysis with six structurally different PA heliotrine, echimidine, lasiocarpine, senecionine, senkirkine, and platyphylline after subacute treatment of rats

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ADAMTS13 deficiency promotes platelet accumulation in pyrrolizidine alkaloids-induced liver injury

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Gene expression changes in rat liver induced by 6 PA

Project description:Pyrrolizidine alkaloids (PA) are secondary plant metabolites that occur as food and feed contaminants. Acute and subacute PA poisoning can lead to severe liver damage in humans and animals. Chronic exposure to low levels of PA can induce liver cirrhosis and liver cancer. However, it is not well understood which transcriptional changes are induced by PA and whether all hepatotoxic PA, regardless of their structure, induce similar responses. Therefore, a 28-day subacute rat feeding study was performed with six structurally different PA heliotrine, echimidine, lasiocarpine, senecionine, senkirkine, and platyphylline, administered at not acutely toxic doses from 0.1 to 3.3 mg/kg body weight. This dose range is relevant for humans, since consumption of contaminated tea may result in doses of ~8 µg/kg in adults and cases of PA ingestion by contaminated food was reported for infants with doses up to 3 mg/kg. ALT and AST were not increased in all treatment groups. Whole genome microarray analyses revealed pronounced effects on gene expression in the high-dose treatment groups resulting in a set of 36 commonly regulated genes. However, platyphylline, the only 1,2-saturated and therefore presumably non-hepatotoxic PA, did not induce significant expression changes. Biological functions identified to be affected by high dose treatments (3.3 mg/kg body weight) comprise cell cycle regulation associated with DNA damage response. These functions were found to be affected by all analyzed 1,2-unsaturated PA. Transcriptomic analysis with six structurally different PA heliotrine, echimidine, lasiocarpine, senecionine, senkirkine, and platyphylline after subacute treatment of rats

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ADAMTS13 deficiency promotes platelet accumulation in pyrrolizidine alkaloids-induced liver injury

Project description:ADAMTS13 deficiency promotes platelet accumulation in pyrrolizidine alkaloids-induced liver injury

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Next generation sequencing analysis of primary rat lung fibroblast, primary rat lung alveolar type 2 cell and a novel 10-4A rat lung cell line transcriptomes

Project description:Purpose: We report the application of single-molecule-based sequencing technology for high-throughput profiling of a novel 10-4A rat lung fibroblast cell line and compared the transcriptome to freshly isolated primary rat lung fibroblasts and freshly isolated primary rat lung alveolar type 2 cells.

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Blood microRNA signatures serve as potential diagnostic biomarkers for hepatic sinusoidal obstruction syndrome caused by Gynura japonica containing pyrrolizidine alkaloids

Project description:Background & Aims: Gynura japonica-induced hepatic sinusoidal obstruction syndrome (HSOS) is closely related with pyrrolizidine alkaloids (PAs) and the prevalence is on the rise worldwide in recent years. However, there is no effective therapy for PA-induced HSOS in clinic, which is partially caused by the failure of quick diagnosis. The aim of the present study was to identify blood miRNAs signatures as the potential biomarkers for PA-induced HSOS in clinic. Methods: Microarray-based miRNA profiling was performed on blood samples of the discovery cohort, i.e. 9 HSOS patients and 9 healthy donors. The differentially expressed miRNAs were further confirmed using a validation cohort of 20 independent HSOS patients. In addition, rat model was also established by orally administration of total alkaloids extract (TA) from G. japonica to investigate the association of miRNAs biomarkers with the progression of HSOS. Bioinformatic analysis, including GO and KEGG enrichment analyses, receiver operating characteristics curve (ROC) analysis, correlation analysis, etc., were conducted to evaluate the accuracy of the potential miRNA biomarkers. Results: Three miRNAs, namely miR-148a-3p, miR-362-5p, and miR-194-5p, were over-expressed in PA-induced HSOS patients and rats. They were positively related to the severity of liver injury and displayed considerable diagnostic accuracy for HSOS patients with areas under the curve (AUC) over 0.87. Conclusions: In summary, the present study demonstrated that 3 miRNAs, i.e. hsa-miR-148a-3p, hsa-miR-362-5p, and hsa-miR-194-5p, might serve as potential biomarkers for PA-induced HSOS in clinic. Conclusions: In summary, the present study demonstrated that 3 miRNAs, i.e. hsa-miR-148a-3p, hsa-miR-362-5p, and hsa-miR-194-5p, might serve as potential biomarkers for PA-induced HSOS in clinic.

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