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. 2016 Apr 22;13(6):4995–5004. doi: 10.3892/mmr.2016.5161

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Copyright: © Lin et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Secretion of IL-8 in ASMCs was induced by TNF-α. This was determined using enzyme-linked immunosorbent assay. ^*P<0.05 vs. ASMCs from smoke-exposed rats with TNF-α stimulation and without lentivirus vector treatment; ^#P<0.05 vs. ASMCs from normal rats with TNF-α stimulation and lentivirus vector treatment; ^##P<0.01 vs. ASMCs from normal rats with TNF-α stimulation and without lentivirus vector treatment; ^###P<0.001 vs. ASMCs from normal rats without TNF-α stimulation or lentivirus vector treatment. Data are presented as the mean ± standard error of the mean of eight independent experiments. IL-8, interleukin-8; TRPM7, transient receptor potential cation channel subfamily M member 7; shRNA, short hairpin RNA; TNF-α, tumor necrosis factor-α; ASMCs, airway smooth muscle cells.