期刊
ONCOTARGET
卷 8, 期 43, 页码 73579-73589出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.20568
关键词
IFITM3; characterization; anti-inflammation; TLR4 signaling pathway; lipopolysaccharide; Immunology and Microbiology Section; Immune response; Immunity
资金
- National Key Research and Development Program of China [2016YFD0500503]
- National Natural Science Fund [31470120]
- Genetical modified Grant from Agricultural Ministry [2014ZX0801015B]
- Grant from the Ministry of Agriculture [2011-G35]
- Natural Science Fund of Henan Province [17A230016, 112102310705, 15A230022, 14A230010, 152300410070, 15A230017]
- Zhengzhou City Natural Science Fund [141PPTGG407]
IFITM3 is involved in cell adhesion, apoptosis, immune, and antivirus activity. Furthermore, IFITM3 gene has been considered as a preferential marker for inflammatory diseases, and positive correlation to pathological grades. Therefore, we assumed that IFITM3 was regulated by different signal pathways. To better understand IFITM3 function in inflammatory response, we cloned swine IFITM3 gene, and detected IFITM3 distribution in tissues, as well as characterized this gene. Results indicated that the length of swine IFITM3 gene was 438 bp, encoding 145 amino acids. IFITM3 gene expression abundance was higher in spleen and lungs. Moreover, we next constructed the eukaryotic expression vector PBIFM3 and transfected into PK15 cells, finally obtained swine IFITM3 gene stable expression cell line. Meanwhile, we explored the effects of LPS on swine IFITM3 expression. Results showed that LPS increased IFITM3 mRNA abundance and exhibited time-dependent effect for LPS treatment. To further demonstrate the mechanism that IFITM3 regulated type I IFNs production, we also detected the important molecules expression of TLR4 signaling pathway. In transfected and non-transfected IFITM3 PK15 cells, LPS exacerbated the relative expression of TLR4-NF kappa B signaling molecules. However, the IFITM3 overexpression suppressed the inflammatory development of PK15 cells. In conclusion, these data indicated that the overexpression of swine IFITM3 could decrease the inflammatory response through TLR4 signaling pathway, and participate in type I interferon production. These findings may lead to an improved understanding of the biological function of IFITM3 in inflammation.
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