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ADAM17 介导肺上皮细胞中 MMP9 的表达。

ADAM17 mediates MMP9 expression in lung epithelial cells.

机构信息

Department of Respiratory Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China.

出版信息

PLoS One. 2013;8(1):e51701. doi: 10.1371/journal.pone.0051701. Epub 2013 Jan 14.

DOI:10.1371/journal.pone.0051701
PMID:23341882
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3544892/
Abstract

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.

摘要

目的在于研究脂多糖（LPS）诱导的肿瘤坏死因子（TNF）-α/核因子-κB（NF-κB）信号在肺腺癌细胞中基质金属蛋白酶 9（MMP9）表达中的作用，并探讨靶向解整合素金属蛋白酶 17（ADAM17）基因的慢病毒 RNAi 对 LPS 诱导的 MMP9 表达的影响。结果发现，LPS 诱导 A549 细胞 MMP9 表达呈剂量和时间依赖性增加（p<0.05）。吡咯烷二硫代氨基甲酸盐（PDTC）和 TNFR1 阻断肽（TNFR1BP）显著抑制 LPS 诱导的 A549 细胞 MMP9 表达（p<0.05）。TNFR1BP 显著抑制 LPS 诱导的 TNF-α 产生（p<0.05）。PDTC 和 TNFR1BP 均显著抑制 LPS 诱导的 IκBα 磷酸化和磷酸化 p65 蛋白表达（p<0.05），同时细胞质中 IκBα 水平显著升高（p<0.05）。慢病毒介导的 RNA 干扰（RNAi）显著抑制 A549 细胞中 ADAM17 的表达。慢病毒介导的 ADAM17 RNAi 靶向抑制上清液中 TNF-α 的产生（p<0.05），而细胞内 TNF-α 水平升高（p<0.05）。慢病毒 ADAM17 RNAi 抑制 LPS 诱导的 MMP9 表达、IκBα 磷酸化和磷酸化 p65 蛋白表达（p<0.05）。PDTC 显著抑制 TNF-α 诱导的 MMP9 表达、IκBα 磷酸化和磷酸化 p65 蛋白表达（p<0.05）。结论：靶向 ADAM17 的慢病毒 RNAi 通过抑制 TNF-α/NF-κB 信号通路下调 LPS 诱导的肺上皮细胞 MMP9 表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/5c55b1ffa331/pone.0051701.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/f2ccd00b1002/pone.0051701.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/e45030e75bae/pone.0051701.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/991d038b933c/pone.0051701.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/a8356a66ac6e/pone.0051701.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/5c55b1ffa331/pone.0051701.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/f2ccd00b1002/pone.0051701.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/e45030e75bae/pone.0051701.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/991d038b933c/pone.0051701.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/a8356a66ac6e/pone.0051701.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d336/3544892/5c55b1ffa331/pone.0051701.g005.jpg

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