tetano
Editor, Senior Moderator
Biomed Pharmacother. 2016 Sep 6;83:1464-1470. doi: 10.1016/j.biopha.2016.08.049. [Epub ahead of print]
[h=1]MicroRNA 34a contributes to virus-mediated apoptosis through binding to its target gene Bax in influenza A virus infection.[/h] Fan N[SUP]1[/SUP], Wang J[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]OBJECTIVE:[/h] Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types. However, molecular mechanism of cell apoptosis induced by influenza A virus is not well understood. The present study was aimed to investigate the molecular mechanism of miR-34a involved in influenza A virus induced apoptosis.
[h=4]METHODS:[/h] Firstly, microRNA array was used to select miRNAs involved in influenza A virus infection. Then, Luciferase reporter assay and western blot were carried to determine the target gene of miR-34a. Finally, miR-34a mimic was transfected in influenza A virus-infected A549 cells, and western blot was used to test the function of miR-34a and its target gene in in influenza A virus infection.
[h=4]RESULTS:[/h] miR-34a was found significantly down-regulated in influenza A virus-infected A549 cells and was further confirmed by qRT-PCR in vitro and in vivo (P<0.01). Next, transfection miR-34 mimic/inhibitor in influenza A virus-infected A549 cells showed that overexpression of miR-34a could inhibit influenza virus-induced apoptosis. Furthermore, target prediction analysis revealed that miR-34a complemented to the 3'-UTR of Bax mRNA. Luciferase reporter assay and western blot confirm that miR-34a directly targeted Bax. Moreover, we detected influenza virus infection enhanced the luciferase reporter translational activity in A549 cells transfected with the construct with Bax 3'-UTR encoding miR-34a binding site. However, western blot analysis showed that the up-regulation of Bax protein level was significantly reversed by overexpression miR-34a.
[h=4]CONCLUSION:[/h] It is, therefore, concluded that influenza virus infection regulated pro-apoptotic Bax expression through miR-34a downregulation, which might be the partial mechanism of influenza virus-induced cell apoptosis.
Copyright ? 2016 Elsevier Masson SAS. All rights reserved.
[h=4]KEYWORDS:[/h] Bax; Cell apoptosis; Influenza A virus; miR-34a
PMID: 27610823 DOI: 10.1016/j.biopha.2016.08.049
[PubMed - as supplied by publisher]
[h=1]MicroRNA 34a contributes to virus-mediated apoptosis through binding to its target gene Bax in influenza A virus infection.[/h] Fan N[SUP]1[/SUP], Wang J[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]OBJECTIVE:[/h] Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types. However, molecular mechanism of cell apoptosis induced by influenza A virus is not well understood. The present study was aimed to investigate the molecular mechanism of miR-34a involved in influenza A virus induced apoptosis.
[h=4]METHODS:[/h] Firstly, microRNA array was used to select miRNAs involved in influenza A virus infection. Then, Luciferase reporter assay and western blot were carried to determine the target gene of miR-34a. Finally, miR-34a mimic was transfected in influenza A virus-infected A549 cells, and western blot was used to test the function of miR-34a and its target gene in in influenza A virus infection.
[h=4]RESULTS:[/h] miR-34a was found significantly down-regulated in influenza A virus-infected A549 cells and was further confirmed by qRT-PCR in vitro and in vivo (P<0.01). Next, transfection miR-34 mimic/inhibitor in influenza A virus-infected A549 cells showed that overexpression of miR-34a could inhibit influenza virus-induced apoptosis. Furthermore, target prediction analysis revealed that miR-34a complemented to the 3'-UTR of Bax mRNA. Luciferase reporter assay and western blot confirm that miR-34a directly targeted Bax. Moreover, we detected influenza virus infection enhanced the luciferase reporter translational activity in A549 cells transfected with the construct with Bax 3'-UTR encoding miR-34a binding site. However, western blot analysis showed that the up-regulation of Bax protein level was significantly reversed by overexpression miR-34a.
[h=4]CONCLUSION:[/h] It is, therefore, concluded that influenza virus infection regulated pro-apoptotic Bax expression through miR-34a downregulation, which might be the partial mechanism of influenza virus-induced cell apoptosis.
Copyright ? 2016 Elsevier Masson SAS. All rights reserved.
[h=4]KEYWORDS:[/h] Bax; Cell apoptosis; Influenza A virus; miR-34a
PMID: 27610823 DOI: 10.1016/j.biopha.2016.08.049
[PubMed - as supplied by publisher]