Characterization and anti-inflammation role of swine IFITM3 gene
Identifieur interne : 000F23 ( Main/Exploration ); précédent : 000F22; suivant : 000F24Characterization and anti-inflammation role of swine IFITM3 gene
Auteurs : He-Ping Li [République populaire de Chine] ; Pei-Ge Chen [République populaire de Chine] ; Fu-Tao Liu [République populaire de Chine] ; He-Shui Zhu [République populaire de Chine] ; Xian-Qin Jiao [République populaire de Chine] ; Kai Zhong [République populaire de Chine] ; Yu-Jie Guo [République populaire de Chine] ; Guang-Ming Zha [République populaire de Chine] ; Li-Qiang Han [République populaire de Chine] ; Wei-Fei Lu [République populaire de Chine] ; Yue-Ying Wang [République populaire de Chine] ; Guo-Yu Yang [République populaire de Chine]Source :
- Oncotarget [ 1949-2553 ] ; 2017.
Abstract
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-NFκB 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.
Url:
DOI: 10.18632/oncotarget.20568
PubMed: 29088728
PubMed Central: 5650283
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>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-NFκB 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.</p>
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</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, He Ping" sort="Li, He Ping" uniqKey="Li H" first="He-Ping" last="Li">He-Ping Li</name>
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<name sortKey="Guo, Yu Jie" sort="Guo, Yu Jie" uniqKey="Guo Y" first="Yu-Jie" last="Guo">Yu-Jie Guo</name>
<name sortKey="Han, Li Qiang" sort="Han, Li Qiang" uniqKey="Han L" first="Li-Qiang" last="Han">Li-Qiang Han</name>
<name sortKey="Jiao, Xian Qin" sort="Jiao, Xian Qin" uniqKey="Jiao X" first="Xian-Qin" last="Jiao">Xian-Qin Jiao</name>
<name sortKey="Liu, Fu Tao" sort="Liu, Fu Tao" uniqKey="Liu F" first="Fu-Tao" last="Liu">Fu-Tao Liu</name>
<name sortKey="Lu, Wei Fei" sort="Lu, Wei Fei" uniqKey="Lu W" first="Wei-Fei" last="Lu">Wei-Fei Lu</name>
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<name sortKey="Zha, Guang Ming" sort="Zha, Guang Ming" uniqKey="Zha G" first="Guang-Ming" last="Zha">Guang-Ming Zha</name>
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</tree>
</affiliations>
</record>
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