Academic Journal

Activation of Adhesion GPCR EMR2/ADGRE2 Induces Macrophage Differentiation and Inflammatory Responses via Gα16/Akt/MAPK/NF-κB Signaling Pathways

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Activation of Adhesion GPCR EMR2/ADGRE2 Induces Macrophage Differentiation and Inflammatory Responses via Gα16/Akt/MAPK/NF-κB Signaling Pathways
Συγγραφείς: I, K-Y, Huang, Y-S, Hu, C-H, Tseng, W-Y, Cheng, C-H, Stacey, M, Gordon, S, Chang, G-W, Lin, H-H
Στοιχεία εκδότη: Frontiers Media
Έτος έκδοσης: 2026
Συλλογή: Oxford University Research Archive (ORA)
Περιγραφή: EMR2/ADGRE2 is a human myeloid-restricted adhesion G protein-coupled receptor critically implicated in vibratory urticaria, a rare type of allergy caused by vibration-induced mast cell activation. In addition, EMR2 is also highly expressed by monocyte/macrophages and has been linked to neutrophil migration and activation. Despite these findings, little is known of EMR2-mediated signaling and its role in myeloid biology. In this report, we show that activation of EMR2 via a receptor-specific monoclonal antibody promotes the differentiation of human THP-1 monocytic cell line and induces the expression of pro-inflammatory mediators, including IL-8, TNF-α, and MMP-9. Using specific signaling inhibitors and siRNA knockdowns, biochemical and functional analyses reveal that the EMR2-mediated signaling is initiated by Gα16, followed by the subsequent activation of Akt, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and nuclear factor kappa-light-chain-enhancer of activated B cells. Our results demonstrate a functional role for EMR2 in the differentiation and inflammatory activation of human monocytic cells and provide potential targets for myeloid cell-mediated inflammatory disorders
Τύπος εγγράφου: article in journal/newspaper
Γλώσσα: English
Relation: https://doi.org/10.3389/fimmu.2017.00373
DOI: 10.3389/fimmu.2017.00373
Διαθεσιμότητα: https://doi.org/10.3389/fimmu.2017.00373
https://ora.ox.ac.uk/objects/uuid:41701417-10cd-4fa3-a857-749b2a61e020
Rights: info:eu-repo/semantics/openAccess ; CC Attribution (CC BY)
Αριθμός Καταχώρησης: edsbas.EC35E1F0
Βάση Δεδομένων: BASE