Journal
CELLULAR SIGNALLING
Volume 26, Issue 6, Pages 1204-1212Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2014.02.013
Keywords
MicroRNA; Apoptosis; STAT3; Bim; Macrophage
Categories
Funding
- Natural Basic Research Program of China [2010CB530001]
- National Natural Science Foundation of China [81101272]
Ask authors/readers for more resources
In order to accomplish their life cycles, intracellular pathogens, including the apicomplexan Toxoplasma gondii, subvert the innate apoptotic response of infected host cells. However, the precise mechanisms of parasite interference with the apoptotic pathway remain unclear. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level. Using T. gondii strain TgCtwh3, which was isolated from fends and possesses the predominant genotype China 1 (ToxoDB(#)9) in China, we analyzed the miRNA expression profile of human macrophages challenged with TgCtwh3. The results showed that miR-17-92 miRNA expression was significantly increased and Bim was decreased in TgCtwh3-infected cells. Database analysis of miR-17-92 miRNAs revealed the potential binding sites in the 3'UTR of Bim, one of the crucial effectors of pro-apoptosis. Furthermore, we demonstrated that the promoter of the miR-17-92 gene cluster which encodes miRNAs was transactivated through the promoter binding of the STAT3 following TgCtwh3 infection. Taken together, we describe a novel STAT3-miR-17-92-Bim pathway, thus providing a mechanistic explanation for inhibition of apoptosis of host cells following Toxoplasma infection. (C) 2014 Elsevier Inn All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available