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Advances in Purinergic Signaling

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

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 1493

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Guest Editor
Estudos Biológicos e Clínicos em Patologias Humanas, Universidade Federal da Fronteira Sul, Coordenação Acadêmica, Fronteira Sul, Chapecó 89812000, SC, Brazil
Interests: autoimmune diseases; neurodegenerative diseases; purinergic system; inflammatory processes and oxidative stress
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Special Issue Information

Dear Colleagues, 

Proposed in 1972, purinergic signaling is characterized by the relationship between signaling components, receptors, and specific enzymes. The purinergic system is characterized by the action of extracellular nucleotides and nucleosides that are degraded by the action of several ectonucleotidases. ATP is an intracellular energy molecule, but it can be released from various types of cells after damage. Thus, after release, it can activate receptors or be rapidly decomposed by ectonucleotidases. Purinergic signaling receptors are classified into two main groups: P1 nucleoside receptors and P2 purinoceptors. All cells have components of the purinergic system and can release nucleotides in a controlled situation. It is now established that changes in purinergic signaling are involved in the therapy of many diseases, in addition to being related to the effects of physical exercise and nutraceutical molecules on the body. This Special Issue aims to present and discuss the advancement of research and innovative therapies involving the purinergic system and diseases with a high impact on society, such as diabetes, hypertension, atherosclerosis, heart disease, cancer, and chronic kidney disease, neurological diseases, such as epilepsy, and neurodegenerative ones, such as Alzheimer's and Parkinson's diseases as well as multiple sclerosis, with the possibility of involving communicable and chronic diseases emerging.

Dr. Margarete Dulce Bagatini
Guest Editor

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Keywords

  • purinergic receptors
  • ectonucleotidases
  • nucleotides
  • nucleoside
  • ATP

Published Papers (1 paper)

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Research

21 pages, 3866 KiB  
Article
Ca2+ Dynamics of Gap Junction Coupled and Uncoupled Deiters’ Cells in the Organ of Corti in Hearing BALB/c Mice
by Louise Moysan, Fruzsina Fazekas, Adam Fekete, László Köles, Tibor Zelles and Eszter Berekméri
Int. J. Mol. Sci. 2023, 24(13), 11095; https://doi.org/10.3390/ijms241311095 - 4 Jul 2023
Cited by 1 | Viewed by 1173
Abstract
ATP, as a paracrine signalling molecule, induces intracellular Ca2+ elevation via the activation of purinergic receptors on the surface of glia-like cochlear supporting cells. These cells, including the Deiters’ cells (DCs), are also coupled by gap junctions that allow the propagation of [...] Read more.
ATP, as a paracrine signalling molecule, induces intracellular Ca2+ elevation via the activation of purinergic receptors on the surface of glia-like cochlear supporting cells. These cells, including the Deiters’ cells (DCs), are also coupled by gap junctions that allow the propagation of intercellular Ca2+ waves via diffusion of Ca2+ mobilising second messenger IP3 between neighbouring cells. We have compared the ATP-evoked Ca2+ transients and the effect of two different gap junction (GJ) blockers (octanol and carbenoxolone, CBX) on the Ca2+ transients in DCs located in the apical and middle turns of the hemicochlea preparation of BALB/c mice (P14–19). Octanol had no effect on Ca2+ signalling, while CBX inhibited the ATP response, more prominently in the middle turn. Based on astrocyte models and using our experimental results, we successfully simulated the Ca2+ dynamics in DCs in different cochlear regions. The mathematical model reliably described the Ca2+ transients in the DCs and suggested that the tonotopical differences could originate from differences in purinoceptor and Ca2+ pump expressions and in IP3–Ca2+ release mechanisms. The cochlear turn-dependent effect of CBX might be the result of the differing connexin isoform composition of GJs along the tonotopic axis. The contribution of IP3-mediated Ca2+ signalling inhibition by CBX cannot be excluded. Full article
(This article belongs to the Special Issue Advances in Purinergic Signaling)
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