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賀西南醫(yī)科大學(xué)附屬中醫(yī)醫(yī)院應(yīng)用PriCells產(chǎn)品/技術(shù)服務(wù)

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賀西南醫(yī)科大學(xué)附屬中醫(yī)醫(yī)院應(yīng)用PriCells產(chǎn)品/技術(shù)服務(wù)發(fā)表文章!


Overexpression of the long noncoding RNA TUG1 protects against cold-induced injury of mouse livers by inhibiting apoptosis and inflammation.
FEBS J. 2016 Apr;283(7):1261-74. doi: 10.1111/febs.13660. Epub 2016 Mar 2.
Su S1, Liu J1, He K1, Zhang M1, Feng C1, Peng F1, Li B1, Xia X1.

1Department of Hepatobiliary Surgery, The Affiliated Hospital of Luzhou Medical College, Sichuan Province, China.


Abstract

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. Overexpression of TUG1 attenuated cold-induced apoptosis in mouse hepatocytes and liver sinusoidal endothelial cells LSECs, in part by blocking mitochondrial apoptosis and endoplasmic reticulum (ER) stress pathways. Moreover, TUG1 attenuated apoptosis, inflammation, and oxidative stress in vivo in livers subjected to cold storage. Overexpression 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.


MIC-CELL-0054;PriCells





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