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Updated: Feb 11, 2026

In Vivo Luminal Measurement of Distension-Evoked Urothelial ATP Release in Rodents
Published on: September 7, 2022
Mechanisms of ATP Release by Inflammatory Cells
Michel Dosch1,2, Joël Gerber3,4, Fadi Jebbawi5,6
1Department for Visceral Surgery and Medicine, Bern University Hospital, University of Bern, CH-3010 Bern, Switzerland. michel.dosch@dbmr.unibe.ch.
Abstract:
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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