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The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes

The prokineticin (PK) family, prokineticin 1 and Bv8/prokineticin 2 (PROK2), initially discovered as regulators of gastrointestinal motility, interacts with two G protein-coupled receptors, PKR1 and PKR2, regulating important biological functions such as circadian rhythms, metabolism, angiogenesis,...

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Autores principales: Lattanzi, Roberta, Severini, Cinzia, Maftei, Daniela, Saso, Luciano, Badiani, Aldo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956973/
https://www.ncbi.nlm.nih.gov/pubmed/33732160
http://dx.doi.org/10.3389/fphar.2021.640441
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author Lattanzi, Roberta
Severini, Cinzia
Maftei, Daniela
Saso, Luciano
Badiani, Aldo
author_facet Lattanzi, Roberta
Severini, Cinzia
Maftei, Daniela
Saso, Luciano
Badiani, Aldo
author_sort Lattanzi, Roberta
collection PubMed
description The prokineticin (PK) family, prokineticin 1 and Bv8/prokineticin 2 (PROK2), initially discovered as regulators of gastrointestinal motility, interacts with two G protein-coupled receptors, PKR1 and PKR2, regulating important biological functions such as circadian rhythms, metabolism, angiogenesis, neurogenesis, muscle contractility, hematopoiesis, immune response, reproduction and pain perception. PROK2 and PK receptors, in particular PKR2, are widespread distributed in the central nervous system, in both neurons and glial cells. The PROK2 expression levels can be increased by a series of pathological insults, such as hypoxia, reactive oxygen species, beta amyloid and excitotoxic glutamate. This suggests that the PK system, participating in different cellular processes that cause neuronal death, can be a key mediator in neurological/neurodegenerative diseases. While many PROK2/PKRs effects in physiological processes have been documented, their role in neuropathological conditions is not fully clarified, since PROK2 can have a double function in the mechanisms underlying to neurodegeneration or neuroprotection. Here, we briefly outline the latest findings on the modulation of PROK2 and its cognate receptors following different pathological insults, providing information about their opposite neurotoxic and neuroprotective role in different pathological conditions.
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spelling pubmed-79569732021-03-16 The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes Lattanzi, Roberta Severini, Cinzia Maftei, Daniela Saso, Luciano Badiani, Aldo Front Pharmacol Pharmacology The prokineticin (PK) family, prokineticin 1 and Bv8/prokineticin 2 (PROK2), initially discovered as regulators of gastrointestinal motility, interacts with two G protein-coupled receptors, PKR1 and PKR2, regulating important biological functions such as circadian rhythms, metabolism, angiogenesis, neurogenesis, muscle contractility, hematopoiesis, immune response, reproduction and pain perception. PROK2 and PK receptors, in particular PKR2, are widespread distributed in the central nervous system, in both neurons and glial cells. The PROK2 expression levels can be increased by a series of pathological insults, such as hypoxia, reactive oxygen species, beta amyloid and excitotoxic glutamate. This suggests that the PK system, participating in different cellular processes that cause neuronal death, can be a key mediator in neurological/neurodegenerative diseases. While many PROK2/PKRs effects in physiological processes have been documented, their role in neuropathological conditions is not fully clarified, since PROK2 can have a double function in the mechanisms underlying to neurodegeneration or neuroprotection. Here, we briefly outline the latest findings on the modulation of PROK2 and its cognate receptors following different pathological insults, providing information about their opposite neurotoxic and neuroprotective role in different pathological conditions. Frontiers Media S.A. 2021-03-01 /pmc/articles/PMC7956973/ /pubmed/33732160 http://dx.doi.org/10.3389/fphar.2021.640441 Text en Copyright © 2021 Lattanzi, Severini, Maftei, Saso and Badiani. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Lattanzi, Roberta
Severini, Cinzia
Maftei, Daniela
Saso, Luciano
Badiani, Aldo
The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title_full The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title_fullStr The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title_full_unstemmed The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title_short The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes
title_sort role of prokineticin 2 in oxidative stress and in neuropathological processes
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956973/
https://www.ncbi.nlm.nih.gov/pubmed/33732160
http://dx.doi.org/10.3389/fphar.2021.640441
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