Korean J Physiol Pharmacol 2022; 26(3): 175-182
Published online May 1, 2022 https://doi.org/10.4196/kjpp.2022.26.3.175
Copyright © Korean J Physiol Pharmacol.
Hwa-Yong Ham#, Shin-Hae Kang#, and Dong-Keun Song*
Department of Pharmacology, Hallym University College of Medicine, Chuncheon 24252, Korea
Correspondence to:Dong-Keun Song
E-mail: dksong@hallym.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Translocation of azurophil granules is pivotal for bactericidal activity of neutrophils, the first-line defense cells against pathogens. Previously, we reported that lysophosphatidylcholine (LPC), an endogenous lipid, enhances bactericidal activity of human neutrophils via increasing translocation of azurophil granules. However, the precise mechanism of LPC-induced azurophil granule translocation was not fully understood. Treatment of neutrophil with LPC significantly increased CD63 (an azurophil granule marker) surface expression. Interestingly, cytochalasin B, an inhibitor of action polymerization, blocked LPC-induced CD63 surface expression. LPC increased F-actin polymerization. LPC-induced CD63 surface expression was inhibited by both a Rho specific inhibitor, Tat-C3 exoenzyme, and a Rho kinase (ROCK) inhibitor, Y27632 which also inhibited LPC-induced F-actin polymerization. LPC induced Rho-GTP activation. NSC23766, a Rac inhibitor, however, did not affect LPC-induced CD63 surface expression. Theses results suggest a novel regulatory mechanism for azurophil granule translocation where LPC induces translocation of azurophil granules via Rho/ROCK/F-actin polymerization pathway.
Keywords: Azurophil granule, Lysophosphatidylcholine, Neutrophil, Translocation
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