Inflammation
During inflammation, MSP exerts a dual function, both stimulatory and inhibitory, on macrophages. Stimulatory functions include its ability to induce macrophage spreading, migration, phagocytosis and the production of cytokines. However, MSP inhibits lipopolysaccharide-induced production of inflammatory mediators, such as inducible NO synthase, cyclooxygenase-2, and prostaglandin E2. These suppressive effects are mediated by RON-transduced signals that block LPS-induced activation of NF-κB pathways (Wang et al., 2002; Kretschmann et al., 2010).

Wound healing
MSP/RON signaling is involved at various steps of wound healing process. MSP promotes keratinocyte migration in mouse wound models and in wound healing assays in vitro. In experimental excisional wounds in rats, expression levels of MSP and RON within the wound were highest between 7 and 21 days. In a lung injury model, the function of MSP/RON appears to be necessary to suppress NF-κB activation and RON deficient mice exhibited increased lung injury and significantly decreased survival times (Kretschmann et al., 2010). However, MSP deficient mice do not show any defects in a skin wound healing model, suggesting that functional redundancies exist in the wound healing process (Bezerra et al., 1998). In a gentamicin(GM)-induced nephropathy model, MSP attenuates GM-induced inflammation and apoptosis by inhibition of the MAPKs/NF-κB signaling pathways (Lee et al., 2013).