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Endotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation.

Although the neutrophil recruitment cascade during inflammation has been well described, the molecular players that halt neutrophil chemotaxis remain unclear. In this study, we found that lipopolysaccharide (LPS) was a potent stop signal for chemotactic neutrophil migration. Treatment with an antago... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America April 25, 2017, Vol.114(17), pp.4483-4488
Main Author: Wang, Xu
Other Authors: Qin, Weiting , Xu, Xiaohan , Xiong, Yuyun , Zhang, Yisen , Zhang, Huafeng , Sun, Bingwei
Format: Electronic Article Electronic Article
Language: English
Subjects:
ATP
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1616752114
Link: http://search.proquest.com/docview/1886751455/?pq-origsite=primo
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recordid: proquest1886751455
title: Endotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation.
format: Article
creator:
  • Wang, Xu
  • Qin, Weiting
  • Xu, Xiaohan
  • Xiong, Yuyun
  • Zhang, Yisen
  • Zhang, Huafeng
  • Sun, Bingwei
subjects:
  • Adenosine Triphosphate–Physiology
  • Autocrine Communication–Physiology
  • Chemotaxis–Genetics
  • Connexin 43–Metabolism
  • Endotoxins–Pharmacology
  • Gene Expression Regulation–Physiology
  • HL-60 Cells–Pharmacology
  • Humans–Physiology
  • Lipopolysaccharides–Physiology
  • Myosin Light Chains–Physiology
  • Neutrophils–Physiology
  • Phosphorylation–Physiology
  • Receptors, Purinergic P2x1–Physiology
  • Signal Transduction–Physiology
  • Connexin 43
  • Endotoxins
  • Gja1 Protein, Human
  • Lipopolysaccharides
  • Myosin Light Chains
  • Receptors, Purinergic P2x1
  • Adenosine Triphosphate
  • ATP
  • Chemotaxis
  • Endotoxin
  • Myosin Light Chain
  • Neutrophil
ispartof: Proceedings of the National Academy of Sciences of the United States of America, April 25, 2017, Vol.114(17), pp.4483-4488
description: Although the neutrophil recruitment cascade during inflammation has been well described, the molecular players that halt neutrophil chemotaxis remain unclear. In this study, we found that lipopolysaccharide (LPS) was a potent stop signal for chemotactic neutrophil migration. Treatment with an antagonist of the ATP receptor (P2X1) in primary human neutrophils or knockout of the P2X1 receptor in neutrophil-like differentiated HL-60 (dHL-60) cells recovered neutrophil chemotaxis. Further observations showed that LPS-induced ATP release through connexin 43 (Cx43) hemichannels was responsible for the activation of the P2X1 receptor and the subsequent calcium influx. Increased intracellular calcium stopped neutrophil chemotaxis by activating myosin light chain (MLC) through the myosin light chain kinase (MLCK)-dependent pathway. Taken together, these data identify a previously unknown function of LPS-induced autocrine ATP signaling in inhibiting neutrophil chemotaxis by enhancing MLC phosphorylation, which provides important evidence that stoppage of neutrophil chemotaxis at infectious foci plays a key role in the defense against invading pathogens.
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1616752114
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleEndotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation.
creatorWang, Xu ; Qin, Weiting ; Xu, Xiaohan ; Xiong, Yuyun ; Zhang, Yisen ; Zhang, Huafeng ; Sun, Bingwei
contributorWang, Xu (correspondence author) ; Wang, Xu (record owner)
ispartofProceedings of the National Academy of Sciences of the United States of America, April 25, 2017, Vol.114(17), pp.4483-4488
identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1616752114
subjectAdenosine Triphosphate–Physiology ; Autocrine Communication–Physiology ; Chemotaxis–Genetics ; Connexin 43–Metabolism ; Endotoxins–Pharmacology ; Gene Expression Regulation–Physiology ; HL-60 Cells–Pharmacology ; Humans–Physiology ; Lipopolysaccharides–Physiology ; Myosin Light Chains–Physiology ; Neutrophils–Physiology ; Phosphorylation–Physiology ; Receptors, Purinergic P2x1–Physiology ; Signal Transduction–Physiology ; Connexin 43 ; Endotoxins ; Gja1 Protein, Human ; Lipopolysaccharides ; Myosin Light Chains ; Receptors, Purinergic P2x1 ; Adenosine Triphosphate ; ATP ; Chemotaxis ; Endotoxin ; Myosin Light Chain ; Neutrophil
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descriptionAlthough the neutrophil recruitment cascade during inflammation has been well described, the molecular players that halt neutrophil chemotaxis remain unclear. In this study, we found that lipopolysaccharide (LPS) was a potent stop signal for chemotactic neutrophil migration. Treatment with an antagonist of the ATP receptor (P2X1) in primary human neutrophils or knockout of the P2X1 receptor in neutrophil-like differentiated HL-60 (dHL-60) cells recovered neutrophil chemotaxis. Further observations showed that LPS-induced ATP release through connexin 43 (Cx43) hemichannels was responsible for the activation of the P2X1 receptor and the subsequent calcium influx. Increased intracellular calcium stopped neutrophil chemotaxis by activating myosin light chain (MLC) through the myosin light chain kinase (MLCK)-dependent pathway. Taken together, these data identify a previously unknown function of LPS-induced autocrine ATP signaling in inhibiting neutrophil chemotaxis by enhancing MLC phosphorylation, which provides important evidence that stoppage of neutrophil chemotaxis at infectious foci plays a key role in the defense against invading pathogens.
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