Ontology highlight
ABSTRACT:
PROVIDER: PRJNA791714 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17317400_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR17317401_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR17317402_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR17317303_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR17317304_subreads.fastq.gz | Fastqsanger.gz |
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Project description:Hepatic injury provoked by cold storage is a major problem affecting liver transplantation, as exposure to cold induces apoptosis in hepatic tissues. Long noncoding RNAs (lncRNAs) are increasingly understood to regulate apoptosis, but the contribution of lncRNAs to cold-induced liver injury remains unknown. Using RNA-seq, we determined the differential lncRNA expression profile in mouse livers after cold storage and found that expression of the lncRNA TUG1 was significantly down-regulated. Over-expression of TUG1 attenuated cold-induced apoptosis in mouse hepatocytes and liver sinusoidal endothelial cells LSECs, in part by blocking mitochondrial apoptosis and ER stress pathways. Moreover, TUG1 attenuated apoptosis, inflammation and oxidative stress in vivo in livers subjected to cold storage. Over-expression of TUG1 also improved hepatocyte function and prolonged hepatic graft survival rates in mice. These results suggest that the lncRNA TUG1 exerts a protective effect against cold-induced liver damage by inhibiting apoptosis in mice, and suggests a potential role for TUG1 as a target for the prevention of cold-induced liver damage in liver transplantation.
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