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Figure 7 | Intensive Care Medicine Experimental

Figure 7

From: Genetic and pharmacologic inhibition of Tpl2 kinase is protective in a mouse model of ventilator-induced lung injury

Figure 7

ERK1/2 phosphorylation. (A) The histograms are representative of p-ERK1/2 fluorescence intensity of BALF CD11c positive cells (alveolar macrophages) from non-ventilated mice (n = 6), and from wild-type and Tpl2-deficient mice exposed to either 60 min of normal tidal volume ventilation (n = 4 per group) or 30 min of normal tidal volume ventilation followed by 30 min of high tidal volume ventilation (n = 4 per group), with or without treatment with a Tpl2 inhibitor given 5 min prior to high tidal ventilation. BALF cells stained with isotype control are also depicted. ERK1/2 phosphorylation, as indicated by mean fluorescent intensity (MFI), was higher in WT mice subjected to high VT ventilation than in WT control mice and WT mice ventilated with normal VT *p < 0.05. ERK1/2 phosphorylation was also higher in WT mice subjected to high VT ventilation than in similarly ventilated Tpl2-/-mice and WT mice treated with the Tpl2 inhibitor *p < 0.05. (B) Representative Western blot analysis for phosphorylated and total ERK1/2 of lung homogenates from non-ventilated mice (n = 4 per group) and from WT and Tpl2-/-mice (n = 4 per group) exposed to 30 min of high tidal volume ventilation. Mechanical ventilation was associated with increased ERK1/2 phosphorylation in lungs of both WT and Tpl2-/-mice compared to genotype-matched control mice, *p < 0.05.

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