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. 2020 Jul 9;10(19):8528–8540. doi: 10.7150/thno.46002

Figure 6.

Figure 6

Inhibition of ROCK abolished the phosphorylation of LIMK1/2 and the improvement in wound healing caused by high [Cl-]i in 16HBE14o- cells. A) Western blot analysis images of LIMK1/2 phosphorylation in 16HBE14o- cells after 1 h of incubation with buffers with various chloride concentrations. B) Phosphorylation of LIMK1/2 was measured in 16HBE14o- cells after 1 h of treatment with high [Cl-]i in the presence of Y-27632 (1, 10, and 30 µM). C-D) Phosphorylation of LIMK1/2 was measured in 16HBE14o- cells after 1 h of treatment with CLICs (CFTRinh-172 and IAA94) in the presence of Y-27632 (10 µM). The signal in each lane was quantified by using ImageJ software, and the ratios of p-LIMK1/2/LIMK1/2 to β-actin were determined (n = 3 independent experiments, *P < 0.05; **P < 0.01). E) 16HBE14o- cells were wounded, and wound-healing rates were monitored over a 24 h period under high [Cl-]i conditions in the presence of Y-27632 (10 µM) for 1 h (n = 3 independent experiments; #P < 0.05). Data are presented as mean ± SD.