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. 2013 Aug 21;8(8):e74201. doi: 10.1371/journal.pone.0074201

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© 2013 Shi et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

PMC Copyright notice

NHE-1 interacts with ERM proteins and functions as an anchoring point for actin filament, contributing to membrane protrusion and microglial movement. BK, a chemoattractant produced in injured brain tissues, can induce microglial migration. BK activates the G-protein coupled BK receptor and results in the downstream signaling cascade including activation of phospholipase C (PLC), synthesis of inositol triphosphate (IP₃) and diacylglycerol (DAG), and activation of protein kinase C (PKC). BK stimulates microglial NHE-1 activity to maintain an alkaline pH_i in lamellipodia, which facilitates the pH_i-sensitive actin binding proteins ADF/cofilin function during microglial movement. In addition, NHE-1 mediated Na⁺ influx triggers the NCX_rev operation and Ca²⁺ _i rise, which further facilities ERM activation and actin accumulation. Taken together, NHE-1 plays an important role in microglial migration.