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Glycine Induces Migration of Microglial BV-2 Cells via SNAT-Mediated Cell Swelling
VerfasserKittl, M. ; Dobias, H. ; Beyreis, M. ; Kiesslich, T. ; Mayr, C. ; Gaisberger, M. ; Ritter, M. ; Kerschbaum, H.H. ; Jakab, M.
Erschienen in
Cellular Physiology and Biochemistry, Basel, 2018, Jg. 2018, H. 50, S. 1460-1473
ErschienenBasel : Karger, 2018
SpracheEnglisch
DokumenttypAufsatz in einer Zeitschrift
ISSN1421-9778
URNurn:nbn:at:at-ubs:3-10430 Persistent Identifier (URN)
DOI10.1159/000494646 
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Glycine Induces Migration of Microglial BV-2 Cells via SNAT-Mediated Cell Swelling [2.16 mb]
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Zusammenfassung (Englisch)

The neutral, non-essential amino acid glycine has manifold functions and effects under physiological and pathophysiological conditions. Besides its function as a neurotransmitter in the central nervous system, glycine also exerts immunomodulatory effects and as an osmolyte it participates in cell volume regulation. During phagocytosis, glycine contributes to (local) cell volume-dependent processes like lamellipodium formation. Similar to the expansion of the lamellipodium we assume that glycine also affects the migration of microglial cells in a cell volume-dependent manner. Methods: Mean cell volume (MCV) and cell migration were determined using flow cytometry and trans-well migration assays, respectively. Electrophysiological recordings of the cell membrane potential (Vmem) and swelling-dependent chloride (Cl-) currents (IClswell, VSOR, VRAC) were performed using the whole-cell patch clamp technique. Results: In the murine microglial cell line BV-2, flow cytometry analysis revealed that glycine (5 mM) increases the MCV by 9%. The glycine-dependent increase in MCV was suppressed by the partial sodium-dependent neutral amino acid transporter (SNAT) antagonist MeAIB and augmented by the Cl- current blocker DCPIB. Electrophysiological recordings showed that addition of glycine activates a Cl- current under isotonic conditions resembling features of the swelling-activated Cl- current (IClswell). The cell membrane potential (Vmem) displayed a distinctive time course after glycine application; initially, glycine evoked a rapid depolarization mediated by Na+-coupled glycine uptake via SNAT, followed by a further gradual depolarization, which was fully suppressed by DCPIB. Interestingly, glycine significantly increased migration of BV-2 cells, which was suppressed by MeAIB, suggesting that SNAT is involved in the migration process of microglial cells. Conclusion: We conclude that glycine acts as a chemoattractant for microglial cells presumably by a cell volume-dependent mechanism involving SNAT-mediated cell swelling.

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