tetano
Editor, Senior Moderator
Biochem Biophys Res Commun. 2014 Jun 19. pii: S0006-291X(14)01133-4. doi: 10.1016/j.bbrc.2014.06.059. [Epub ahead of print]
Induction of the cellular miR-29c by influenza virus inhibits the innate immune response through protection of A20 mRNA.
Zhang X1, Dong C1, Sun X1, Li Z2, Zhang M1, Guan Z1, Duan M3.
Author information
Abstract
Influenza A viruses (IAV) are negative-sense, single-stranded, segmented RNA viruses, which primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. The human miR-29 family of miRNAs has three mature members, miR-29a, miR-29b, and miR-29c. Recent studies have revealed that miR-29 is involved in regulation of the innate and adaptive immune responses. However, the function of miR-29 in the immune response to IAV infection remains to be further explored. Our previous study has shown that miR-29 family members are up-regulated during IAV infection, especially miR-29c. Here we report that miR-29c is involved in inhibition of IAV-induced innate immune responses. We found that posttranscriptional regulation was involved in IAV-induced A20 expression in A549 cells. Consistent with a previous report, miR-29c functionally protected A20 transcripts in A549 cells. Overexpression of miR-29c with miR-29c mimic enhanced IAV-induced A20 protein expression and conversely that miR-29c inhibitor significantly blocked IAV-induced A20 protein expression in A549 cells. Furthermore, functional results showed that IAV-induced miR-29c expression correlated with decreased NF-κB activity and expression of several antiviral and proinflammatory cytokines via up-regulation of A20. Together, the findings indicate a new role of miR-29c in IAV infection and suggest its induction may contribute to counteract the innate immune response.
Copyright ? 2014. Published by Elsevier Inc.
KEYWORDS:
A20; Influenza A virus; Innate immune response; miR-29c
PMID:
24953694
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24953694
Induction of the cellular miR-29c by influenza virus inhibits the innate immune response through protection of A20 mRNA.
Zhang X1, Dong C1, Sun X1, Li Z2, Zhang M1, Guan Z1, Duan M3.
Author information
Abstract
Influenza A viruses (IAV) are negative-sense, single-stranded, segmented RNA viruses, which primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. The human miR-29 family of miRNAs has three mature members, miR-29a, miR-29b, and miR-29c. Recent studies have revealed that miR-29 is involved in regulation of the innate and adaptive immune responses. However, the function of miR-29 in the immune response to IAV infection remains to be further explored. Our previous study has shown that miR-29 family members are up-regulated during IAV infection, especially miR-29c. Here we report that miR-29c is involved in inhibition of IAV-induced innate immune responses. We found that posttranscriptional regulation was involved in IAV-induced A20 expression in A549 cells. Consistent with a previous report, miR-29c functionally protected A20 transcripts in A549 cells. Overexpression of miR-29c with miR-29c mimic enhanced IAV-induced A20 protein expression and conversely that miR-29c inhibitor significantly blocked IAV-induced A20 protein expression in A549 cells. Furthermore, functional results showed that IAV-induced miR-29c expression correlated with decreased NF-κB activity and expression of several antiviral and proinflammatory cytokines via up-regulation of A20. Together, the findings indicate a new role of miR-29c in IAV infection and suggest its induction may contribute to counteract the innate immune response.
Copyright ? 2014. Published by Elsevier Inc.
KEYWORDS:
A20; Influenza A virus; Innate immune response; miR-29c
PMID:
24953694
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24953694