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Rat liver stem cells

ABSTRACT: Generation of rat liver organoid lines and their engraftment in a rat model of liver failure

PROVIDER: PRJEB9910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR964947.fastq.gz	Fastqsanger.gz
	ERR964948.fastq.gz	Fastqsanger.gz
	ERR964949.fastq.gz	Fastqsanger.gz
	ERR964950.fastq.gz	Fastqsanger.gz
	ERR964951.fastq.gz	Fastqsanger.gz

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Gene expression profiles of rat liver tissues after carbon tetrachloride treatment

Project description:Acute hepatic failure (AHF) usually occurs due to the rapid necrosis of liver cells or serious liver injury induced by a variety of pathogenic factors. We used Rat Genome 230 2.0 microarray to further highlight the rat liver tissues after carbon tetrachloride treatment.

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Targeting GPX4-mediated ferroptosis alleviates liver injury in a rat model of intestinal failure-associated liver disease

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Human iPSC-liver organoid transplant reduces fibrosis by immunomodulation

Project description:Donor organ shortage for transplant is a serious problem worldwide. Organoid culture technology, which allows the generation of complex organs from stem cells, provides a potential solution. We previously reported in vivo vascularization of human induced pluripotent stem cell (hiPSC)-derived liver buds (LBs) and subsequent improved survival of recipient mice with acute liver failure1,2. Here, we show that mid-gestational fetal liver tissue can generate de novo liver when grafted onto the surface of host livers and improve survival and liver functions in a model of liver failure. Next, we created complex fetal liver-like organoids (LOs) by a fusion of hiPSC-LBs to induce static cell-cell interactions, and show that these contain hepatocytes, vasculature, and bile duct after transplantation. Fused hiPSC-LOs show superior liver functions compared to hiPSC-LBs and improve survival and functions of liver failure model upon transplantation. Finally, transplant of fused hiPSC-LOs ameliorates liver fibrosis, a symptom of liver cirrhosis which leads to organ dysfunction, through their immunomodulatory effects especially on macrophage polarization that plays an important role in the regulation of liver fibrosis3–5. Taken together, our results suggest that hiPSC-LO transplant could be a promising therapeutic option for liver failure patients in the near future

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Human and rat liver microtissue

Project description:Cross species comparison of liver enzyme induction caused by phenobarbital treatment of human and rat liver microtissues.

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Targeting GPX4-mediated ferroptosis alleviates liver injury in a rat model of intestinal failure-associated liver disease

Project description:Background: Intestinal failure-associated liver disease (IFALD) is a common complication of long-term parenteral nutrition (PN) that is associated with significant morbidity and mortality. Ferroptosis, as an iron-dependent regulated cell death, has been shown to play an important role in the development of several liver diseases. This study focuses on investigating whether the ferroptosis phenomenon is present in TPN-induced IFALD and further exploring the potential regulatory mechanisms. Methods: Ferroptosis hallmarkers were measured in children with short bowel syndrome (SBS) who had long-term PN use and caused IFALD. Sprague-Dawley (SD) rats were used to establish a rat model of IFALD with a concomitant ferroptosis inhibition intervention using liproxstain-1. The mir-431 lineage was identified as a potential upstream regulatory mir-RNA by mir-RNA sequencing. HepG2 and 293T cell line was used to demonstrate that mir-431 regulates ferroptosis through the GPX4 pathway at the cellular level in vitro. Results: Ferroptosis is upregulated in liver of children with IFALD. Liproxstain-1 downregulates ferroptosis in a rat model of IFALD and attenuates hepatic steatosis through the lipid metabolism pathway. In vitro HepG2 and 293T cell experiments reveal that mir-431 affects ferroptosis by regulating GPX4 protein. Conclusions: Ferroptosis plays an important role in the development of IFALD. Liproxstain-1 inhibits ferroptosis and attenuates hepatic steatosis in a rat model of IFALD through the lipid metabolism pathway. Mir-431 negatively regulates GPX4 protein-induced ferroptosis.

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Rat liver treated by PCN

Project description:The combination analyses of transcriptomics, proteomics, phosphoproteomics, and metabolomics in rat liver after repeated oral doses of PXR agonist, PCN, for 7 days were conducted to understand the roles for PXR on non-genotoxic signaling and energy homeostasis. mRNA and proteins in homogenate supernatant, membrane, and cytosolic fractions prepared from the liver were analyzed.

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