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. 2021 Apr 23;22(9):4411. doi: 10.3390/ijms22094411

Figure 2.

Figure 2

Simplified illustration of biological effects of S1PR2 in inflammatory bone loss diseases. S1PR2 couples with Gi, Gq, and G12/13 proteins, which manipulate multiple signaling pathways affecting inflammatory diseases. First, S1PR2 controls PI3K, NF-κB, and MAPKs signaling pathways induced by LPS, influencing IL-1β, IL-6, TNF-α inflammatory cytokine release. Second, S1PR2 modulates Sphk1 and S1P generation induced by inflammation. Third, S1PR2 manipulates chemotaxis of osteoclast precursors from blood circulation to bone and soft tissues by modulating inflammatory cytokine and S1P generation. Fourth, S1PR2 controls podosome components (F-actin, integrins, Src, PI3K) induced by RANKL and modulates the adhesion and fusion of osteoclast precursors. S1PR2 possibly interacts with Gi, Gq, and G12/13 proteins, RANKL adaptor protein TRAF6, and TLR4 adaptor protein MyD88 in lipid rafts after stimulation by RANKL or LPS.