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Model Establishment of Mice with Oxaliplatin-induced Hepatic Sinusoidal Obstruction Syndrome

ABSTRACT: Model Establishment of Mice with Oxaliplatin-induced Hepatic Sinusoidal Obstruction Syndrome

PROVIDER: PRJNA872386 | ENA |

REPOSITORIES: ENA

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Model Establishment of Mice with Oxaliplatin-induced Hepatic Sinusoidal Obstruction Syndrome

Project description:To further explore to mechanisms of oxaliplatin-induced hepatic sinusodial obstruction syndrome, we established a mouse model of OXA-induced HSOS and the difference of mRNA expression level between normal mice and model mice was detected.

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Transcription profiling by array of human liver to investigate pathways of Oxaliplatin Related Sinusoidal Obstruction

Project description:Sinusoidal obstruction syndrome (SOS; formerly veno-occlusive disease) is a well-established complication of hematopoietic stem cell transplantation, pyrrolizidine alkaloid intoxication, and widely used chemotherapeutic agents such as oxaliplatin. It is associated with substantial morbidity and mortality. Pathogenesis of SOS in humans is poorly understood. To explore its molecular mechanisms, we used Affymetrix U133 Plus 2.0 microarrays to investigate the gene expression profile of 11 human livers with oxaliplatin-related SOS and compared it to 12 matched controls. Hierarchical clustering analysis showed that profiles from SOS and controls formed distinct clusters. To identify functional networks and gene ontologies, data were analyzed by the Ingenuity Pathway Analysis Tool. A total of 913 genes were differentially expressed in SOS: 613 being upregulated and 300 downregulated. Reverse transcriptase-PCR results showed excellent concordance with microarray data. Pathway analysis showed major gene upregulation in six pathways in SOS compared with controls: acute phase response (notably interleukin 6), coagulation system (Serpine1, THBD, and VWF), hepatic fibrosis/hepatic stellate cell activation (COL3a1, COL3a2, PDGF-A, TIMP1, and MMP2), and oxidative stress. Angiogenic factors (VEGF-C) and hypoxic factors (HIF1A) were upregulated. The most significant increase was seen in CCL20 mRNA. In conclusion, oxaliplatin-related SOS can be readily distinguished according to morphologic characteristics but also by a molecular signature. Global gene analysis provides new insights into mechanisms underlying chemotherapy-related hepatotoxicity in humans and potential targets relating to its diagnosis, prevention, and treatment. Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS. This dataset is part of the TransQST collection.

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Identification of molecular pathways involved in oxaliplatin-associated sinusoidal dilatation

Project description:Oxaliplatin-based chemotherapy for colorectal liver metastases (CRLM) can result in vascular liver lesions such as sinusoidal dilatations. Physiopathology remains unclear and variability between patients suggests that there is individual susceptibility. A better understanding of the molecular mechanisms of oxaliplatin liver toxicity may allow to identification of biomarkers and adaptation of chemotherapy delivery. non-tumor frozen liver samples were obtained from patients operated on for CRLM after an exclusive oxaliplatin-based chemotherapy. Gene-expression profiles were first analyzed by microarray on a selected population of 20 patients; 9 patients with severe sinusoidal dilatation (SD) after a short period of chemotherapy and 10 patients without any sinusoidal dilatation after a long period of chemotherapy. These were compared with a control group of 5 patients without any chemotherapy and lesions. This dataset is part of the TransQST collection.

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Project description:The purpose of the study is to determine whether anticoagulant use (i.e. salicylates, clopidogrel, low-molecular weight heparin, or coumarin derivates) is able to prevent the development of the sinusoidal obstruction syndrome secondary to oxaliplatin-based neoadjuvant chemotherapy in patients suffering from colorectal liver metastases.

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Identification of molecular pathways involved in oxaliplatin-associated sinusoidal dilatation

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Next generation RNAseq from human hepatic sinusoidal endothelial cells (EC) and mouse sinusoidal EC plated on soft vs hard gels

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

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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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Project description:Unravelling the genetic determinants of sinusoidal obstruction syndrome: an integrative multi-omics approach

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