tetano
Editor, Senior Moderator
Biochem Biophys Res Commun. 2012 Jul 28. [Epub ahead of print]
Induction of the cellular microRNA-29c by influenza virus contributes to virus-mediated apoptosis through repression of antiapoptotic factors BCL2L2.
Guan Z, Shi N, Song Y, Zhang X, Zhang M, Duan M.
Source
Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun, 130062, PR China.
Abstract
Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types, which contributes to cellular and organ dysfunction. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. Recent studies have revealed that miR-29c is involved in a variety of biological processes, including apoptosis. However, its role in influenza A virus infection is not well understood. Here, we report that miR-29c is involved in apoptosis induced by influenza A virus infection. We found that several apoptosis-associated miRNAs were stimulated in influenza A virus-infected A549 cells by miRNA array analysis. Within those, miR-29c was significantly up-regulated. In silico target prediction analysis revealed complementarity of miR-29c to the 3'-untranslated region (UTR) of BCL2L2 mRNA. Targeting of BCL2L2 3'UTR by miR-29c was determined by luciferase assay. Functional overexpression of miR-29c with miR-29c precursor inhibited BCL2L2 protein expression. Tansfection of miR-29c inhibitor abolished both suppression of BCL2L2 protein expression and A549 cells apoptosis induced by influenza A virus. Moreover, BCL2L2 overexpression rescued A549 cell death induced by influenza A virus infection. These findings indicate that miR-29c-mediated BCL2L2 suppression is involved in influenza virus-induced cell death in A549 cells.
Copyright ? 2012 Elsevier Inc. All rights reserved.
PMID:
22850539
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22850539
Induction of the cellular microRNA-29c by influenza virus contributes to virus-mediated apoptosis through repression of antiapoptotic factors BCL2L2.
Guan Z, Shi N, Song Y, Zhang X, Zhang M, Duan M.
Source
Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun, 130062, PR China.
Abstract
Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types, which contributes to cellular and organ dysfunction. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. Recent studies have revealed that miR-29c is involved in a variety of biological processes, including apoptosis. However, its role in influenza A virus infection is not well understood. Here, we report that miR-29c is involved in apoptosis induced by influenza A virus infection. We found that several apoptosis-associated miRNAs were stimulated in influenza A virus-infected A549 cells by miRNA array analysis. Within those, miR-29c was significantly up-regulated. In silico target prediction analysis revealed complementarity of miR-29c to the 3'-untranslated region (UTR) of BCL2L2 mRNA. Targeting of BCL2L2 3'UTR by miR-29c was determined by luciferase assay. Functional overexpression of miR-29c with miR-29c precursor inhibited BCL2L2 protein expression. Tansfection of miR-29c inhibitor abolished both suppression of BCL2L2 protein expression and A549 cells apoptosis induced by influenza A virus. Moreover, BCL2L2 overexpression rescued A549 cell death induced by influenza A virus infection. These findings indicate that miR-29c-mediated BCL2L2 suppression is involved in influenza virus-induced cell death in A549 cells.
Copyright ? 2012 Elsevier Inc. All rights reserved.
PMID:
22850539
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22850539