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MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ. | LitMetric

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ.

RNA

Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, 114 Taiwan Institute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan

Published: March 2015

AI Article Synopsis

Article Abstract

In hepatitis B virus (HBV)-replicating hepatocytes, miR-130a expression was significantly reduced. In a reciprocal manner, miR-130a reduced HBV replication by targeting at two major metabolic regulators PGC1α and PPARγ, both of which can potently stimulate HBV replication. We proposed a positive feed-forward loop between HBV, miR-130a, PPARγ, and PGC1α. Accordingly, HBV can significantly enhance viral replication by reducing miR-130a and increasing PGC1α and PPARγ. NF-κB/p65 can strongly stimulate miR-130a promoter, while miR-130a can promote NF-κB/p65 protein level by reducing PPARγ and thus NF-κB/p65 protein degradation. We postulated another positive feed-forward loop between miR-130a and NF-κB/p65 via PPARγ. During liver inflammation, NF-κB signaling could contribute to viral clearance via its positive effect on miR-130a transcription. Conversely, in asymptomatic HBV carriers, persistent viral infection could reduce miR-130a and NF-κB expression, leading to dampened inflammation and immune tolerance. Finally, miR-130a could contribute to metabolic homeostasis by dual targeting PGC1α and PPARγ simultaneously.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338335PMC
http://dx.doi.org/10.1261/rna.048744.114DOI Listing

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