ADAM17 Mediates MMP9 Expression in Lung Epithelial CellsReportar como inadecuado




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The purposes were to study the role of lipopolysaccharide LPS-induced tumor necrosis factor TNF-α-nuclear factor-κB NF-κB signaling in matrix metalloproteinase 9 MMP9 expression in A549 cells and to investigate the effects of lentivirus-mediated RNAi targeting of the disintegrin and metalloproteinase 17 ADAM17 gene on LPS-induced MMP9 expression. MMP9 expression induced by LPS in A549 cells was significantly increased in a dose- and time-dependent manner p<0.05. Pyrrolidine dithiocarbamate PDTC and a TNFR1 blocking peptide TNFR1BP significantly inhibited LPS-induced MMP9 expression in A549 cells p<0.05. TNFR1BP significantly inhibited LPS-induced TNF-α production p<0.05. Both PDTC and TNFR1BP significantly inhibited the phosphorylation of IκBα and expression of phosphorylation p65 protein in response to LPS p<0.05, and the level of IκBα in the cytoplasm was significantly increased p<0.05. Lentivirus mediated RNA interference RNAi significantly inhibited ADAM17 expression in A549 cells. Lentivirus-mediated RNAi targeting of ADAM17 significantly inhibited TNF-α production in the supernatants p<0.05, whereas the level of TNF-α in the cells was increased p<0.05. Lentiviral ADAM17 RNAi inhibited MMP9 expression, IκBα phosphorylation and the expression of phosphorylation p65 protein in response to LPS p<0.05. PDTC significantly inhibited the expression of MMP9 and the phosphorylation of IκBα, as well as the expression of phosphorylation p65 protein in response to TNF-α p<0.05. Lentiviral RNAi targeting of ADAM17 down-regulates LPS-induced MMP9 expression in lung epithelial cells via inhibition of TNF-α-NF-κB signaling.



Autor: Ya-qing Li, Jian-ping Yan, Wu-lin Xu , Hong Wang, Ying-jie Xia, Hui-jun Wang, Yue-yan Zhu, Xiao-jun Huang

Fuente: http://plos.srce.hr/



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