Send to

Choose Destination
See comment in PubMed Commons below
Inflammation. 2014 Feb;37(1):287-94. doi: 10.1007/s10753-013-9739-3.

Identification of microRNAs dysregulated in CD14 gene silencing RAW264.7 macrophage cells.

Author information

College of Agriculture, Hainan Key Lab of Tropical Animal Reproduction & Breeding and Epidemic Disease Research, Animal Genetic Engineering Key Lab of Haikou, Hainan University, Haidian Island, Haikou, 570228, People's Republic of China.


A cluster of differentiation antigen 14 (CD14) is involved in lipopolysaccharide (LPS)-induced proinflammatory cytokine release and LPS-induced septic shock. MicroRNAs (miRNAs) are short non-coding RNAs that are involved in the epigenetic regulation of cellular process and bacterial infection. Our previous study indicated that siRNA against CD14 effectively inhibited LPS-induced tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 2, interleukin-6 release, and NO production. To identify miRNAs which are affected by CD14 gene silencing and dissect the mechanisms of the attenuating of LPS-induced damaging immune activation more clearly, based on the CD14 knockdown RAW264.7 macrophage cell line established in our previous study, miRNAs expression profiling of CD14 knockdown RAW264.7 cells were analyzed with miRNA microarray and validated by qRT-PCR, the potential targets were predicted and subjected to gene ontology (GO) pathway and biological processes analysis. We demonstrated for the first time that CD14 knockdown significantly changed the expression of 199a-3p, miR-199a-5p, and miR-21-5p in RAW264.7 cells, and significantly enriched GO terms in the predicted target genes of these miRNAs were apoptosis process, immune response, inflammatory response, innate immune response, anti-apoptosis, cytokine production, and cytokine-mediated signaling pathway. These findings may improve our understanding about functional mechanism of miRNAs in the attenuating of LPS-induced damaging immune activation more clearly.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons


    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center