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MicroRNA-19b-3p Modulates Japanese Encephalitis Virus-Mediated Inflammation via Targeting RNF11.

Ashraf U, Zhu B, Ye J, Wan S, Nie Y, Chen Z, Cui M, Wang C, Duan X, Zhang H, Chen H, Cao S - J. Virol. (2016)

Bottom Line: Japanese encephalitis virus (JEV) can invade the central nervous system and consequently induce neuroinflammation, which is characterized by profound neuronal cell damage accompanied by astrogliosis and microgliosis.The pathological features of JEV-induced encephalitis are inflammatory reactions and neurological diseases resulting from glia activation.The present study reveals that miR-19b-3p targets ring finger protein 11 in glia and promotes inflammatory cytokine production by enhancing nuclear factor kappa B activity in these cells.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China Laboratory of Animal Virology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China.

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miR-19b-3p activates NF-κB signaling via targeting RNF11 in JEV-infected astrocytes. U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA (final concentration, 50 nM) for 24 h and then infected with JEV at an MOI of 5 for 36 h. The cytosolic extracts (upper panel) and nuclear extracts (lower panel) were isolated and subjected to immunoblotting with antibodies against RNF11, NF-κB p65, lamin A, and GAPDH. Lamin A was used as a marker for nuclei. GAPDH and lamin A were used as the loading controls. Protein levels were quantified by immunoblot scanning and normalized to the amount of GAPDH or lamin A expression. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
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Figure 8: miR-19b-3p activates NF-κB signaling via targeting RNF11 in JEV-infected astrocytes. U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA (final concentration, 50 nM) for 24 h and then infected with JEV at an MOI of 5 for 36 h. The cytosolic extracts (upper panel) and nuclear extracts (lower panel) were isolated and subjected to immunoblotting with antibodies against RNF11, NF-κB p65, lamin A, and GAPDH. Lamin A was used as a marker for nuclei. GAPDH and lamin A were used as the loading controls. Protein levels were quantified by immunoblot scanning and normalized to the amount of GAPDH or lamin A expression. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Mentions: To substantiate that miR-19b-3p is indeed involved in the regulation of NF-κB signaling through RNF11, U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA and subsequently infected with JEV. As expected, silencing of RNF11 significantly enhanced the accumulation of NF-κB in the nucleus, and these effects were concordant with miR-19b-3p overexpression (Fig. 8). Similar to our previous data, JEV-induced nuclear translocation of NF-κB was decreased by miR-19b-3p inhibitors. However, knockdown of RNF11 rescued the inhibitory effects of miR-19b-3p inhibitors on NF-κB activity (Fig. 8), suggesting that miR-19b-3p activates NF-κB activity via targeting RNF11.


MicroRNA-19b-3p Modulates Japanese Encephalitis Virus-Mediated Inflammation via Targeting RNF11.

Ashraf U, Zhu B, Ye J, Wan S, Nie Y, Chen Z, Cui M, Wang C, Duan X, Zhang H, Chen H, Cao S - J. Virol. (2016)

miR-19b-3p activates NF-κB signaling via targeting RNF11 in JEV-infected astrocytes. U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA (final concentration, 50 nM) for 24 h and then infected with JEV at an MOI of 5 for 36 h. The cytosolic extracts (upper panel) and nuclear extracts (lower panel) were isolated and subjected to immunoblotting with antibodies against RNF11, NF-κB p65, lamin A, and GAPDH. Lamin A was used as a marker for nuclei. GAPDH and lamin A were used as the loading controls. Protein levels were quantified by immunoblot scanning and normalized to the amount of GAPDH or lamin A expression. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 8: miR-19b-3p activates NF-κB signaling via targeting RNF11 in JEV-infected astrocytes. U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA (final concentration, 50 nM) for 24 h and then infected with JEV at an MOI of 5 for 36 h. The cytosolic extracts (upper panel) and nuclear extracts (lower panel) were isolated and subjected to immunoblotting with antibodies against RNF11, NF-κB p65, lamin A, and GAPDH. Lamin A was used as a marker for nuclei. GAPDH and lamin A were used as the loading controls. Protein levels were quantified by immunoblot scanning and normalized to the amount of GAPDH or lamin A expression. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Mentions: To substantiate that miR-19b-3p is indeed involved in the regulation of NF-κB signaling through RNF11, U251 cells were cotransfected with miR-19b-3p inhibitors or control oligonucleotides and siRNF11 or a nonspecific control siRNA and subsequently infected with JEV. As expected, silencing of RNF11 significantly enhanced the accumulation of NF-κB in the nucleus, and these effects were concordant with miR-19b-3p overexpression (Fig. 8). Similar to our previous data, JEV-induced nuclear translocation of NF-κB was decreased by miR-19b-3p inhibitors. However, knockdown of RNF11 rescued the inhibitory effects of miR-19b-3p inhibitors on NF-κB activity (Fig. 8), suggesting that miR-19b-3p activates NF-κB activity via targeting RNF11.

Bottom Line: Japanese encephalitis virus (JEV) can invade the central nervous system and consequently induce neuroinflammation, which is characterized by profound neuronal cell damage accompanied by astrogliosis and microgliosis.The pathological features of JEV-induced encephalitis are inflammatory reactions and neurological diseases resulting from glia activation.The present study reveals that miR-19b-3p targets ring finger protein 11 in glia and promotes inflammatory cytokine production by enhancing nuclear factor kappa B activity in these cells.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China Laboratory of Animal Virology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China.

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Related in: MedlinePlus