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4 results on '"purinergic enzyme"'

1. ENPP1/CD203a-targeting heavy-chain antibody reveals cell-specific expression on human immune cells.

Author

Lorenz, Hannah, Menzel, Stephan, Roshchyna, Nataliia, Albrecht, Birte, Gebhardt, Anna Josephine, Schneider, Enja, Haag, Friedrich, Rissiek, Björn, Oheim, Ralf, Koch-Nolte, Friedrich, Winzer, Riekje, and Tolosa, Eva

Subjects
*IMMUNOREGULATION, *B cells, *ADENINE nucleotides, *MEDICAL sciences, *DENDRITIC cells, *PURINERGIC receptors
Abstract

ENPP1/CD203a is a membrane-bound ectonucleotidase capable of hydrolyzing ATP, cGAMP and other substrates. Its enzymatic activity plays an important role in the balance of extracellular adenine nucleotides and the modulation of purinergic signaling, in soft tissue calcification, and in the regulation of the cGAS/STING pathway. However, a detailed analysis of ENPP1 surface expression on human immune cells has not been performed. Here, we selected VHH domains from human ENPP1-immunized alpacas to generate heavy-chain antibodies targeting ENPP1, and analyzed cell surface expression on all circulating immune cell subsets using flow cytometry. We find high expression of ENPP1 in CD141high conventional dendritic cells (cDC1), while ENPP1 was not detectable on other dendritic cells and monocytes. In the lymphocytic compartment, only CD56bright natural killer cells and mucosal-associated invariant T cells (MAIT) express ENPP1. In contrast, all other T cell subpopulations, CD56dim natural killer cells and B lymphocytes do not or only minimally express ENPP1. In summary, we describe highly cell type-specific expression of ENPP1 in the immune system using a newly generated heavy-chain antibody. This reagent will help to decipher the function of ENPP1 in the regulation of the immune response, allow a quick identification of ENPP1-deficiency and of ENPP1-positive tumors, and constitutes the basis for targeted anti-tumor intervention. [ABSTRACT FROM AUTHOR]

Published
2024
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3. The role of purinergic pathways in the pathophysiology of gut diseases: pharmacological modulation and potential therapeutic applications

Author

Antonioli, Luca, Colucci, Rocchina, Pellegrini, Carolina, Giustarini, Giulio, Tuccori, Marco, Blandizzi, Corrado, Fornai, Matteo, and Sub IRAS Tox ITX (immunotoxicologie)

Subjects
Adenosine, diarrhea, inosine, purinergic receptor, duodenum, phenolsulfonphthalein, immune response, sensory dysfunction, purinergic enzyme, blood flow, Gut, enteritis, chelerythrine, mucosa, pathophysiology, phenolphthalein, tetrodotoxin, gastrointestinal tract function, analgesic agent, hydroxymethylglutaryl coenzyme A reductase kinase, carbachol, unclassified drug, preladenant, 4 [2 [7 amino 2 (2 furyl) 1,2,4 triazolo[2,3 a][1,3,5]triazin 5 ylamino]ethyl]phenol, xanthine, priority journal, hypoxanthine, ileum, visceral pain, Purinergic receptors, motor dysfunction, stomach, review, ticlopidine, adenosine kinase, intestine ischemia, sensory nerve, uric acid, nucleoside derivative, human, neuromuscular function, purinergic transporter, spinorphin, glia cell, intestine, pentobarbital, clopidogrel, suramin, nonhuman, colon, submucosa, disease association, abdominal pain, Intestinal disorders, 3 [[5 (2,3 dichlorophenyl) 1h tetrazol 1 yl]methyl]pyridine, adenosine deaminase, ATP, enzyme, guanosine, enteropathy, inflammation, interstitial cell of Cajal, nucleotide derivative, protein, metabolism, small intestine
Abstract

Gut homeostasis results from complex neuro-immune interactions aimed at triggering stereotypical and specific programs of coordinated mucosal secretion and powerful motor propulsion. A prominent role in the regulation of this highly integrated network, comprising a variety of immune/inflammatory cells and the enteric nervous system, is played by purinergic mediators. The cells of the digestive tract are literally plunged into a "biological sea" of functionally active nucleotides and nucleosides, which carry out the critical task of driving regulatory interventions on cellular functions through the activation of P1 and P2 receptors. Intensive research efforts are being made to achieve an integrated view of the purinergic system, since it is emerging that the various components of purinergic pathways (i.e., enzymes, transporters, mediators and receptors) are mutually linked entities, deputed to finely modulating the magnitude and the duration of purinergic signaling, and that alterations occurring in this balanced network could be intimately involved in the pathophysiology of several gut disorders. This review article intends to provide a critical appraisal of current knowledge on the purinergic system role in the regulation of gastrointestinal functions, considering these pathways as a whole integrated network, which is capable of finely controlling the levels of bioactive nucleotides and nucleosides in the biophase of their respective receptors. Special attention is paid to the mechanisms through which alterations in the various compartments of the purinergic system could contribute to the pathophysiology of gut disorders, and to the possibility of counteracting such dysfunctions by means of pharmacological interventions on purinergic molecular targets. © 2013 Elsevier Inc.

Published
2013

4. The role of purinergic pathways in the pathophysiology of gut diseases: pharmacological modulation and potential therapeutic applications

Subjects
Adenosine, diarrhea, 4 [2 [7 amino 2 (2 furyl) 1, inosine, purinergic receptor, duodenum, phenolsulfonphthalein, immune response, sensory dysfunction, purinergic enzyme, blood flow, Gut, enteritis, chelerythrine, mucosa, pathophysiology, phenolphthalein, tetrodotoxin, 3 a][1, gastrointestinal tract function, 3 dichlorophenyl) 1h tetrazol 1 yl]methyl]pyridine, analgesic agent, hydroxymethylglutaryl coenzyme A reductase kinase, carbachol, unclassified drug, preladenant, xanthine, priority journal, hypoxanthine, ileum, visceral pain, Purinergic receptors, motor dysfunction, stomach, review, ticlopidine, adenosine kinase, intestine ischemia, sensory nerve, uric acid, nucleoside derivative, human, neuromuscular function, purinergic transporter, spinorphin, glia cell, intestine, pentobarbital, clopidogrel, suramin, nonhuman, colon, submucosa, disease association, abdominal pain, Intestinal disorders, 4 triazolo[2, adenosine deaminase, ATP, 5]triazin 5 ylamino]ethyl]phenol, enzyme, guanosine, 3 [[5 (2, enteropathy, inflammation, interstitial cell of Cajal, nucleotide derivative, protein, metabolism, small intestine
Abstract

Gut homeostasis results from complex neuro-immune interactions aimed at triggering stereotypical and specific programs of coordinated mucosal secretion and powerful motor propulsion. A prominent role in the regulation of this highly integrated network, comprising a variety of immune/inflammatory cells and the enteric nervous system, is played by purinergic mediators. The cells of the digestive tract are literally plunged into a "biological sea" of functionally active nucleotides and nucleosides, which carry out the critical task of driving regulatory interventions on cellular functions through the activation of P1 and P2 receptors. Intensive research efforts are being made to achieve an integrated view of the purinergic system, since it is emerging that the various components of purinergic pathways (i.e., enzymes, transporters, mediators and receptors) are mutually linked entities, deputed to finely modulating the magnitude and the duration of purinergic signaling, and that alterations occurring in this balanced network could be intimately involved in the pathophysiology of several gut disorders. This review article intends to provide a critical appraisal of current knowledge on the purinergic system role in the regulation of gastrointestinal functions, considering these pathways as a whole integrated network, which is capable of finely controlling the levels of bioactive nucleotides and nucleosides in the biophase of their respective receptors. Special attention is paid to the mechanisms through which alterations in the various compartments of the purinergic system could contribute to the pathophysiology of gut disorders, and to the possibility of counteracting such dysfunctions by means of pharmacological interventions on purinergic molecular targets. © 2013 Elsevier Inc.

Published
2013
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