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Highly expressed MT ‐ ND 3 positively associated with histological severity of hepatic steatosis
Author(s) -
Wang HanNing,
Chen HongDong,
Chen KaiYun,
Xiao JinFeng,
He Ke,
Xiang GuoAn,
Xie Xin
Publication year - 2014
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12166
Subject(s) - steatosis , lipotoxicity , fatty liver , medicine , oxidative stress , biology , endocrinology , lipid metabolism , pathogenesis , apoptosis , pathology , biochemistry , insulin resistance , disease , insulin
Hepatic steatosis is the accumulation of an excess amount of triglycerides and other fats inside liver cells resulting from abnormal hepatic lipid metabolism. Mitochondrial structural and molecular defects are involved in the progression of hepatic steatosis pathogenesis. Hepatic methylation and transcriptional activity of the mitochondrial‐encoded NADH dehydrogenase ( MT ‐ ND ) play a critical role in the progression of non‐alcoholic fatty liver disease ( NAFLD ). However, the expression of MT ‐ ND 3 in hepatic steatosis has not been extensively studied. In this study, liver specimens were collected from different patients, and were subjected to immunohistochemistry. Primary hepatocytes were treated with oxidative stress, hypoxia, and lipotoxicity to investigate the respective roles of these factors on MT ‐ ND 3 expression and cell apoptosis by western blotting and flow cytometry, respectively. We found that increased MT ‐ ND 3 expression in human hepatic steatosis was positively associated with histological severity of hepatic steatosis. Hypoxia, H 2 O 2 , and saturated fatty acid treatment induced cell apoptosis mediated by mitochondria. These three factors all had effects on MT ‐ ND3 expression in cultured hepatocytes. Taken together, MT ‐ ND3 may play important roles in hepatic steatosis progress. Hypoxia, oxidative stress, and lipotoxicity could all influence expression of MT ‐ ND3 and thus may play a role in the progression of hepatic steatosis.