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Mechanisms of ATP Release by Inflammatory Cells

Extracellular nucleotides (e.g., ATP, ADP, UTP, UDP) released by inflammatory cells interact with specific purinergic P2 type receptors to modulate their recruitment and activation. The focus of this review is on stimuli and mechanisms of extracellular nucleotide release and its consequences during...

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Detalles Bibliográficos
Autores principales: Dosch, Michel, Gerber, Joël, Jebbawi, Fadi, Beldi, Guido
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979498/
https://www.ncbi.nlm.nih.gov/pubmed/29669994
http://dx.doi.org/10.3390/ijms19041222
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author Dosch, Michel
Gerber, Joël
Jebbawi, Fadi
Beldi, Guido
author_facet Dosch, Michel
Gerber, Joël
Jebbawi, Fadi
Beldi, Guido
author_sort Dosch, Michel
collection PubMed
description Extracellular nucleotides (e.g., ATP, ADP, UTP, UDP) released by inflammatory cells interact with specific purinergic P2 type receptors to modulate their recruitment and activation. The focus of this review is on stimuli and mechanisms of extracellular nucleotide release and its consequences during inflammation. Necrosis leads to non-specific release of nucleotides, whereas specific release mechanisms include vesicular exocytosis and channel-mediated release via connexin or pannexin hemichannels. These release mechanisms allow stimulated inflammatory cells such as macrophages, neutrophils, and endothelial cells to fine-tune autocrine/paracrine responses during acute and chronic inflammation. Key effector functions of inflammatory cells are therefore regulated by purinergic signaling in acute and chronic diseases, making extracellular nucleotide release a promising target for the development of new therapies.
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spelling pubmed-59794982018-06-10 Mechanisms of ATP Release by Inflammatory Cells Dosch, Michel Gerber, Joël Jebbawi, Fadi Beldi, Guido Int J Mol Sci Review Extracellular nucleotides (e.g., ATP, ADP, UTP, UDP) released by inflammatory cells interact with specific purinergic P2 type receptors to modulate their recruitment and activation. The focus of this review is on stimuli and mechanisms of extracellular nucleotide release and its consequences during inflammation. Necrosis leads to non-specific release of nucleotides, whereas specific release mechanisms include vesicular exocytosis and channel-mediated release via connexin or pannexin hemichannels. These release mechanisms allow stimulated inflammatory cells such as macrophages, neutrophils, and endothelial cells to fine-tune autocrine/paracrine responses during acute and chronic inflammation. Key effector functions of inflammatory cells are therefore regulated by purinergic signaling in acute and chronic diseases, making extracellular nucleotide release a promising target for the development of new therapies. MDPI 2018-04-18 /pmc/articles/PMC5979498/ /pubmed/29669994 http://dx.doi.org/10.3390/ijms19041222 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Dosch, Michel
Gerber, Joël
Jebbawi, Fadi
Beldi, Guido
Mechanisms of ATP Release by Inflammatory Cells
title Mechanisms of ATP Release by Inflammatory Cells
title_full Mechanisms of ATP Release by Inflammatory Cells
title_fullStr Mechanisms of ATP Release by Inflammatory Cells
title_full_unstemmed Mechanisms of ATP Release by Inflammatory Cells
title_short Mechanisms of ATP Release by Inflammatory Cells
title_sort mechanisms of atp release by inflammatory cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979498/
https://www.ncbi.nlm.nih.gov/pubmed/29669994
http://dx.doi.org/10.3390/ijms19041222
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