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Overexpression of the long noncoding RNA TUG 1 protects against cold‐induced injury of mouse livers by inhibiting apoptosis and inflammation
Author(s) -
Su Song,
Liu Jiang,
He Kai,
Zhang Mengyu,
Feng Chunhong,
Peng Fangyi,
Li Bo,
Xia Xianming
Publication year - 2016
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13660
Subject(s) - apoptosis , cold storage , endoplasmic reticulum , microbiology and biotechnology , biology , inflammation , oxidative stress , hepatocyte , rna , immunology , cancer research , biochemistry , gene , in vitro , horticulture
Hepatic injury provoked by cold storage is a major problem affecting liver transplantation, as exposure to cold induces apoptosis in hepatic tissues. Long noncoding RNA s (lnc RNA s) are increasingly understood to regulate apoptosis, but the contribution of lnc RNA s to cold‐induced liver injury remains unknown. Using RNA ‐seq, we determined the differential lnc RNA expression profile in mouse livers after cold storage and found that expression of the lnc RNA TUG 1 was significantly down‐regulated. Overexpression of TUG 1 attenuated cold‐induced apoptosis in mouse hepatocytes and liver sinusoidal endothelial cells LSEC s, in part by blocking mitochondrial apoptosis and endoplasmic reticulum (ER) stress pathways. Moreover, TUG 1 attenuated apoptosis, inflammation, and oxidative stress in vivo in livers subjected to cold storage. Overexpression of TUG 1 also improved hepatocyte function and prolonged hepatic graft survival rates in mice. These results suggest that the lnc RNA TUG 1 exerts a protective effect against cold‐induced liver damage by inhibiting apoptosis in mice, and suggests a potential role for TUG 1 as a target for the prevention of cold‐induced liver damage in liver transplantation. Databases RNA‐seq data are available from GEO using accession number GSE76609 .