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. 2011 Apr 4;8(4):305–314. doi: 10.1038/cmi.2011.8

Figure 5.

Figure 5

CXCL12 protects lung-accumulated neutrophils of LPS-injured mice from apoptosis through MEK/ERK and PI3K/Akt pathways. (a) Neutrophils were isolated from the mouse lungs at 24 h after LPS instillation. Isolated neutrophils were untreated or pre-incubated with a CXCR4 antagonist then treated CXCL12. Western blot analysis showed that CXCL12 induced the phosphorylation of ERK1/2 and Akt. (b, c) The isolated neutrophils were cultured for 24 h at 37 °C in the presence (white bar) or absence (black bar) of CXCL12 alone or in combination with a MEK1/2 inhibitor (U0126) or a PI3K inhibitor (LY294002). Subsequently, staining with Annexin V and 7-AAD was also performed to detect early apoptotic (Annexin V+7-AAD−; b) cells and late apoptotic/necrotic (Annexin V+7-AAD+; c) cells. Note the suppression of the inhibitory effect of CXCL12 against apoptosis in the presence of MEK1/2 inhibitor or PI3K inhibitor. The values represent mean±s.e.m. (n=6). *P<0.01 versus before culture group and †P<0.01 versus media only group using ANOVA with Scheffé's post hoc test. 7-AAD, 7-aminoactinomycin D; LPS, lipopolysaccharide.