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Special Issue "Dissecting the Purinergic Signaling Puzzle"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 June 2020).

Special Issue Editors

Prof. Raquel Pérez-Sen
Website
Guest Editor
Departamento de Bioquímica y Biología Molecular, Facultad de Veterinaria, Instituto Universitario de Investigación en Neuroquímica (IUIN), Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC), Universidad Complutense Madrid, 28040 Madrid, Spain
Interests: purinergic signaling; P2X receptors; P2Y receptors; neuroprotection; neural cells; protein phosphatases; DUSPs; signaling cascades
Prof. Esmerilda G. Delicado
Website
Guest Editor
Departamento de Bioquímica y Biología Molecular, Facultad de Veterinaria, Instituto Universitario de Investigación en Neuroquímica (IUIN), Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdiSSC), Universidad Complutense Madrid, 28040 Madrid, Spain
Interests: purinergic signaling; P2X receptors; P2Y receptors; neuroprotection; astrocytes; neural cells; protein phosphatases; DUSPs; signaling cascades

Special Issue Information

Dear Colleagues,

Purinergic signaling represents an expanding field involved in the regulation of a plethora of physio-pathological processes in different tissues and systems. One interesting feature that characterizes the purinergic network and makes it more complex and interesting than the rest of neurotransmitter systems is the numerous components integrating into a multistep cascade called “purinome”. In order to better understand the physiological relevance of nucleotide signaling, it should be considered as a whole, having an integrative view of all these elements and their relationships. The purinergic system includes nucleotide and adenosine receptors, and enzymatic and transporter activities interconverting nucleotides and nucleosides and connecting the intra- and extracellular spaces to regulate purinergic messenger availability. The aim of this Special Issue is to cover different key components of the purinergic system, regarding how they interact and work together in a coordinate fashion to shape and modulate the final biological response.

Prof. Raquel Pérez-Sen
Prof. Esmerilda G. Delicado
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • purinergic signaling
  • P2X receptor
  • P2Y receptor
  • adenosine receptor
  • adenosine/nucleoside transporter
  • vesicular nucleotide transporter (VNUT)
  • ectoenzymes
  • nucleotide/nucleoside metabolism
  • purinome
  • intracellular pathways

Published Papers (3 papers)

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Research

Open AccessArticle
Signaling Through Purinergic Receptor P2Y2 Enhances Macrophage IL-1β Production
Int. J. Mol. Sci. 2020, 21(13), 4686; https://doi.org/10.3390/ijms21134686 - 30 Jun 2020
Abstract
The release of nucleotides during necrosis or apoptosis has been described to have both proinflammatory and anti-inflammatory effect on the surrounding cells. Here we describe how low concentrations of UTP and ATP applied during macrophage priming enhance IL-1β production when subsequently the NLRP3 [...] Read more.
The release of nucleotides during necrosis or apoptosis has been described to have both proinflammatory and anti-inflammatory effect on the surrounding cells. Here we describe how low concentrations of UTP and ATP applied during macrophage priming enhance IL-1β production when subsequently the NLRP3 inflammasome is activated in murine resident peritoneal macrophages. Deficiency or pharmacological inhibition of the purinergic receptor P2Y2 reverted the increase of IL-1β release induced by nucleotides. IL-1β increase was found dependent on the expression of Il1b gene and probably involving JNK activity. On the contrary, nucleotides decreased the production of a different proinflammatory cytokines such as TNF-α. These results suggest that nucleotides could shape the response of macrophages to obtain a unique proinflammatory signature that might be relevant in unrevealing specific inflammatory conditions. Full article
(This article belongs to the Special Issue Dissecting the Purinergic Signaling Puzzle)
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Open AccessArticle
Adenosine Deaminase as a Biomarker of Tenofovir Mediated Inflammation in Naïve HIV Patients
Int. J. Mol. Sci. 2020, 21(10), 3590; https://doi.org/10.3390/ijms21103590 - 19 May 2020
Abstract
Plasma levels of adenosine deaminase (ADA), an enzyme that deaminates adenosine to inosine, are increased during inflammation. An increase in ADA activity occurs with lower human immunodeficiency virus (HIV) viral load and higher CD4+ T cell counts. We aimed to investigate the [...] Read more.
Plasma levels of adenosine deaminase (ADA), an enzyme that deaminates adenosine to inosine, are increased during inflammation. An increase in ADA activity occurs with lower human immunodeficiency virus (HIV) viral load and higher CD4+ T cell counts. We aimed to investigate the role of plasma ADA as a biomarker of inflammation in treatment-naïve HIV patients who received tenofovir or another nucleoside analog for comparison. Ninety-two treatment-naïve patients were included in the study and grouped by treatment, i.e., tenofovir disoproxil fumarate (TDF), tenofovir alafenamide (TAF) or Triumeq. ADA activity was measured in plasma and cytokines were analyzed by MILLIPLEX® MAP-Luminex® Technology. Plasma concentration of monocytes and neutrophils was measured at 0, 3, and 12 months post-treatment. Treatment-naïve HIV patients had increased ADA concentrations (over 15 U/L) that decreased after treatment with TAF and Triumeq, though this did not occur in TDF-treated patients. However, all groups exhibited a pro-inflammatory systemic profile at 12 months of treatment. Plasma GM-CSF levels decreased after 12 months of treatment in the TDF group, with a concomitant decrease in blood monocyte count, and a negative correlation with ADA values was found. In conclusion, ADA levels may be modulated by antiretroviral therapy in HIV patients, possibly affecting inflammatory status. Full article
(This article belongs to the Special Issue Dissecting the Purinergic Signaling Puzzle)
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Open AccessArticle
Abnormal Upregulation of GPR17 Receptor Contributes to Oligodendrocyte Dysfunction in SOD1 G93A Mice
Int. J. Mol. Sci. 2020, 21(7), 2395; https://doi.org/10.3390/ijms21072395 - 31 Mar 2020
Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons (MN). Importantly, MN degeneration is intimately linked to oligodendrocyte dysfunction and impaired capacity of oligodendrocyte precursor cells (OPCs) to regenerate the myelin sheath enwrapping and protecting neuronal axons. [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons (MN). Importantly, MN degeneration is intimately linked to oligodendrocyte dysfunction and impaired capacity of oligodendrocyte precursor cells (OPCs) to regenerate the myelin sheath enwrapping and protecting neuronal axons. Thus, improving OPC reparative abilities represents an innovative approach to counteract MN loss. A pivotal regulator of OPC maturation is the P2Y-like G protein-coupled receptor 17 (GPR17), whose role in ALS has never been investigated. In other models of neurodegeneration, an abnormal increase of GPR17 has been invariably associated to myelin defects and its pharmacological manipulation succeeded in restoring endogenous remyelination. Here, we analyzed GPR17 alterations in the SOD1G93A ALS mouse model and assessed in vitro whether this receptor could be targeted to correct oligodendrocyte alterations. Western-blot and immunohistochemical analyses showed that GPR17 protein levels are significantly increased in spinal cord of ALS mice at pre-symptomatic stage; this alteration is exacerbated at late symptomatic phases. Concomitantly, mature oligodendrocytes degenerate and are not successfully replaced. Moreover, OPCs isolated from spinal cord of SOD1G93A mice display defective differentiation compared to control cells, which is rescued by treatment with the GPR17 antagonist montelukast. These data open novel therapeutic perspectives for ALS management. Full article
(This article belongs to the Special Issue Dissecting the Purinergic Signaling Puzzle)
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