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激动剂 TUG-891 抑制小鼠肺泡巨噬细胞的运动和吞噬作用。

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

机构信息

Institute of Basic Medical Sciences, Xi'an Medical University, Xi'an 710021, China.

出版信息

Biomed Res Int. 2020 Feb 20;2020:1706168. doi: 10.1155/2020/1706168. eCollection 2020.

DOI:10.1155/2020/1706168
PMID:32149083
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7056993/
Abstract

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 concentration ([Ca]i), and the ability of phagocytosis were measured. Mouse AM in controls exhibited active movement , and TUG-891 significantly restrained AM movement. Meanwhile, TUG-891 stimulated a quick increase in [Ca]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 store by thapsigargin. The inhibition of AM movement by TUG-891 was eliminated by YM-254890, U73122, thapsigargin, and chelation of cytosolic Ca 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]i but inhibits the motility and phagocytosis via Gq protein/PLC-mediated Ca release from ER Ca store.

摘要

运动和吞噬作用是巨噬细胞的基本功能。虽然已知游离脂肪酸受体 GPR120 在巨噬细胞中表达，并调节细胞因子表达发挥抗炎作用，但 GPR120 激活对巨噬细胞的运动和吞噬作用的影响尚不清楚。在这项研究中，用 GPR120 激动剂 TUG-891 刺激小鼠肺泡巨噬细胞（AM），测量细胞运动、细胞内 Ca 浓度 ([Ca]i) 和吞噬能力的变化。对照小鼠 AM 表现出活跃的运动，而 TUG-891 显著抑制 AM 运动。同时，TUG-891 刺激 AM 中 [Ca]i 的快速增加，该增加可分别被 Gq 蛋白抑制剂 YM-254890、PLC 抑制剂 U73122 或 thapsigargin 耗尽内质网 (ER) Ca 库所阻断。TUG-891 对 AM 运动的抑制作用被 YM-254890、U73122、thapsigargin 和 BAPTA 螯合细胞浆 Ca 所消除。此外，TUG-891 抑制 AM 对荧光微球的吞噬作用，该作用也被 YM-254890、U73122、thapsigargin 和 BAPTA 所阻断。总之，GPR120 在小鼠 AM 中的激活增加 [Ca]i，但通过 Gq 蛋白/PLC 介导的 ER Ca 库中 Ca 释放来抑制运动和吞噬作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/abb80f258808/BMRI2020-1706168.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/1430d7af7f4a/BMRI2020-1706168.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/30030e992d80/BMRI2020-1706168.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/a0406dae61e0/BMRI2020-1706168.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/84ce12578ebb/BMRI2020-1706168.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/860a29b91391/BMRI2020-1706168.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/abb80f258808/BMRI2020-1706168.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/1430d7af7f4a/BMRI2020-1706168.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/30030e992d80/BMRI2020-1706168.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/a0406dae61e0/BMRI2020-1706168.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/84ce12578ebb/BMRI2020-1706168.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/860a29b91391/BMRI2020-1706168.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c9/7056993/abb80f258808/BMRI2020-1706168.006.jpg

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