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. 2015 Apr 17;6(23):19605–19618. doi: 10.18632/oncotarget.3747

Figure 9. Overexpression of ERK5 reverses TS-induced pulmonary EMT alterations in mice.

Figure 9

A. Intratracheal delivery of lentiviral ERK5 expression vector restored ERK5 activation in the lung tissues of mice exposed to TS for 12 weeks, as shown by Western blotting. B. Lentivirus-mediated ERK5 overexpression suppressed TS-induced activation of c-Fos, c-Jun and FosB proteins in mouse lungs. C. Lentivirus-mediated ERK5 overexpression attenuated TS-induced alterations in mRNA expressions of E-cadherin, ZO-1, Vimentin and N-cadherin, as measured by quantitative reverse transcriptase–polymerase chain reaction. D. ERK5 overexpression prevented TS-induced alterations in protein expression of E-cadherin, ZO-1, Vimentin and N-cadherin, as determined by Western blotting. Data are expressed as mean ± SD. *P < 0.05, compared with FA control group; **P < 0.01, compared with FA control group; #P < 0.05, compared with TS-LV-control group; ##P < 0.01, compared with TS-LV-control group. FA = filtered air; TS = tobacco smoke; LV-control = lentiviral control vector; LV-ERK5 = lentiviral vector for ERK5.