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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

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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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Project description:Effect of continuous GH treatment on old rat liver. Male rats, 2-year-old, were treated with vehicle or human GH (0.34 microgram/gram body weight) for 3 weeks. Keywords: response of old rat liver to growth hormone

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