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The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages

Movement and phagocytosis characterize the fundamental actions of macrophages. Although it is known that the free fatty acid receptor GPR120 is expressed in macrophages and regulates cytokine expression to exert anti-inflammatory activities, the effects of GPR120 activation on the motility and phago...

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Autores principales: Su, Xing-Li, Liu, Ying-Guang, Shi, Man, Zhao, Yan-Yan, Liang, Xiang-Yan, Zhang, Li-Jun, Wei, Lan-Lan, Zhao, Yu-Feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7056993/
https://www.ncbi.nlm.nih.gov/pubmed/32149083
http://dx.doi.org/10.1155/2020/1706168
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author Su, Xing-Li
Liu, Ying-Guang
Shi, Man
Zhao, Yan-Yan
Liang, Xiang-Yan
Zhang, Li-Jun
Wei, Lan-Lan
Zhao, Yu-Feng
author_facet Su, Xing-Li
Liu, Ying-Guang
Shi, Man
Zhao, Yan-Yan
Liang, Xiang-Yan
Zhang, Li-Jun
Wei, Lan-Lan
Zhao, Yu-Feng
author_sort Su, Xing-Li
collection PubMed
description Movement and phagocytosis characterize the fundamental actions of macrophages. Although it is known that the free fatty acid receptor GPR120 is expressed in macrophages and regulates cytokine expression to exert anti-inflammatory activities, the effects of GPR120 activation on the motility and phagocytosis of macrophages are not clear. In this study, mouse alveolar macrophages (AM) were stimulated with the GPR120 agonist TUG-891, and the changes in cell motility, intracellular Ca(2+) concentration ([Ca(2+)]i), and the ability of phagocytosis were measured. Mouse AM in controls exhibited active movement in vitro, and TUG-891 significantly restrained AM movement. Meanwhile, TUG-891 stimulated a quick increase in [Ca(2+)]i in AM, which was blocked separately by the Gq protein inhibitor YM-254890, the phospholipase C (PLC) inhibitor U73122, or depletion of endoplasmic reticulum (ER) Ca(2+) store by thapsigargin. The inhibition of AM movement by TUG-891 was eliminated by YM-254890, U73122, thapsigargin, and chelation of cytosolic Ca(2+) by BAPTA. Moreover, TUG-891 inhibited AM phagocytosis of fluorescent microspheres, which was also blocked by YM-254890, U73122, thapsigargin, and BAPTA. In conclusion, GPR120 activation in mouse AM increases [Ca(2+)]i but inhibits the motility and phagocytosis via Gq protein/PLC-mediated Ca(2+) release from ER Ca(2+) store.
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spelling pubmed-70569932020-03-08 The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages Su, Xing-Li Liu, Ying-Guang Shi, Man Zhao, Yan-Yan Liang, Xiang-Yan Zhang, Li-Jun Wei, Lan-Lan Zhao, Yu-Feng Biomed Res Int Research Article Movement and phagocytosis characterize the fundamental actions of macrophages. Although it is known that the free fatty acid receptor GPR120 is expressed in macrophages and regulates cytokine expression to exert anti-inflammatory activities, the effects of GPR120 activation on the motility and phagocytosis of macrophages are not clear. In this study, mouse alveolar macrophages (AM) were stimulated with the GPR120 agonist TUG-891, and the changes in cell motility, intracellular Ca(2+) concentration ([Ca(2+)]i), and the ability of phagocytosis were measured. Mouse AM in controls exhibited active movement in vitro, and TUG-891 significantly restrained AM movement. Meanwhile, TUG-891 stimulated a quick increase in [Ca(2+)]i in AM, which was blocked separately by the Gq protein inhibitor YM-254890, the phospholipase C (PLC) inhibitor U73122, or depletion of endoplasmic reticulum (ER) Ca(2+) store by thapsigargin. The inhibition of AM movement by TUG-891 was eliminated by YM-254890, U73122, thapsigargin, and chelation of cytosolic Ca(2+) by BAPTA. Moreover, TUG-891 inhibited AM phagocytosis of fluorescent microspheres, which was also blocked by YM-254890, U73122, thapsigargin, and BAPTA. In conclusion, GPR120 activation in mouse AM increases [Ca(2+)]i but inhibits the motility and phagocytosis via Gq protein/PLC-mediated Ca(2+) release from ER Ca(2+) store. Hindawi 2020-02-20 /pmc/articles/PMC7056993/ /pubmed/32149083 http://dx.doi.org/10.1155/2020/1706168 Text en Copyright © 2020 Xing-Li Su et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Su, Xing-Li
Liu, Ying-Guang
Shi, Man
Zhao, Yan-Yan
Liang, Xiang-Yan
Zhang, Li-Jun
Wei, Lan-Lan
Zhao, Yu-Feng
The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title_full The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title_fullStr The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title_full_unstemmed The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title_short The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
title_sort gpr120 agonist tug-891 inhibits the motility and phagocytosis of mouse alveolar macrophages
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7056993/
https://www.ncbi.nlm.nih.gov/pubmed/32149083
http://dx.doi.org/10.1155/2020/1706168
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