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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells

Fig. 8

Schematic diagram illustrating the proposed immunomodulatory phagocytosis of fAβ42 via PGE2-related signaling mechanism in EMF-stimulated N9 microglial cells. External electromagnetic emission as a physical stimulation directly triggers an initial activation of microglia. Activation of JAK2-STAT3 and MAPKs signaling occurs in parallel with microglial activation, leading to PGE2 synthesis via COX-2-mPGES-1 system. Finally, PGE2 decreased microglial phagocytosis through EP2 receptor. Preventing phosphorylation of JAK2-STAT3 and MAPKs, inhibiting COX-2 activity, or abolishing EP2 activity efficiently ameliorated microglial phagocytosis during EMF stimulation

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