Figure 7. The effects of ephrinA1-mediated activation of EphA2 on the phosphoinositide 3-kinase (PI3K)/Akt signaling pathways in lipopolysaccharide (LPS)-induced lung injury. EphA2-ephrinA1 signaling may contribute to the development of LPS-induced lung injury. Exposure to LPS resulted in activation of the EphA2-ephrinA1 and PI3K/Akt/nuclear factor κB (NF-κB) signaling pathway. EphA2 monoclonal antibody-induced inhibition of EphA2 signaling resulted in decreased PI3K/Akt/NF-κB-dependent inflammatory processes. These results suggested crosstalk between EphA2 signaling and PI3K/Akt/NF-κB signaling in LPS-induced lung injury. TNF-α: tumor necrosis factor α; IL: interleukin.