MicroRNA-221 Regulates FAS-Induced Fulminant Liver Failure

被引:60
作者
Sharma, Amar Deep [1 ]
Narain, Nidhi [2 ]
Haendel, Eva-Maria [3 ]
Iken, Marcus [2 ]
Singhal, Nishant [4 ]
Cathomen, Toni [3 ]
Manns, Michael P.
Schoeler, Hans R. [4 ]
Ott, Michael [2 ]
Cantz, Tobias [4 ]
机构
[1] Hanz Borst Zentrum J11 02 6530, Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Cluster Excellence REBIRTH, D-30625 Hannover, Germany
[2] TWINCORE, Ctr Expt & Clin Infect Res, Hannover, Germany
[3] Hannover Med Sch, Dept Expt Hematol, D-3000 Hannover, Germany
[4] Max Planck Inst Mol Biomed, Munster, Germany
关键词
HEPATOCELLULAR-CARCINOMA; MEDIATED APOPTOSIS; KAPPA-B; BIOGENESIS; EXPRESSION; GROWTH; INJURY; DEATH; CELLS; MICE;
D O I
10.1002/hep.24243
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Death receptor-mediated apoptosis of hepatocytes contributes to hepatitis and fulminant liver failure. MicroRNAs (miRNAs), 19-25 nucleotide-long noncoding RNAs, have been implicated in the posttranscriptional regulation of the various apoptotic pathways. Here we report that global loss of miRNAs in hepatic cells leads to increased cell death in a model of FAS/CD95 receptor-induced apoptosis. miRNA profiling of murine liver identified 11 conserved miRNAs, which were up-regulated in response to FAS-induced fulminant liver failure. We show that ectopic expression of miR-221, one of the highly up-regulated miRNAs in response to apoptosis, protects primary hepatocytes and hepatoma cells from apoptosis. Importantly, in vivo overexpression of miR-221 by adeno-associated virus serotype 8 (AAV8) delays FAS-induced fulminant liver failure in mice. We additionally demonstrate that miR-221 regulates hepatic expression of p53 up-regulated modulator of apoptosis (Puma), a well-known proapoptotic member of the Bcl2 protein family. Conclusion: We identified miR-221 as a potent posttranscriptional regulator of FAS-induced apoptosis. miR-221 may serve as a potential therapeutic target for the treatment of hepatitis and liver failure. (HEPATOLOGY 2011;53:1651-1661)
引用
收藏
页码:1651 / 1661
页数:11
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