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dc.contributor.author
Medrano, Matias
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dc.contributor.author
Pisera Fuster, Antonella
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dc.contributor.author
Bernabeu, Ramon Oscar
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dc.contributor.author
Faillace, Maria Paula
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dc.date.available
2021-09-15T12:19:37Z
dc.date.issued
2020-01
dc.identifier.citation
Medrano, Matias; Pisera Fuster, Antonella; Bernabeu, Ramon Oscar; Faillace, Maria Paula; P2X7 and A2A receptor endogenous activation protects against neuronal death caused by CoCl2-induced photoreceptor toxicity in the zebrafish retina; Wiley-liss, div John Wiley & Sons Inc.; Journal Of Comparative Neurology; 528; 12; 1-2020; 2000-2020
dc.identifier.issn
0021-9967
dc.identifier.uri
http://hdl.handle.net/11336/140368
dc.description.abstract
Injured retinas in mammals do not regenerate and heal with loss of function. The adult retina of zebrafish self-repairs after damage by activating cell-intrinsic mechanisms, which are regulated by extrinsic signal interactions. Among relevant regulatory extrinsic systems, purinergic signaling regulates progenitor proliferation during retinogenesis and regeneration and glia proliferation in proliferative retinopathies. ATP-activated P2X7 (P2RX7) and adenosine (P1R) receptors are involved in the progression of almost all retinopathies leading to blindness. Here, we examined P2RX7 and P1R participation in the retina regenerative response induced by photoreceptor damage caused by a specific dose of CoCl2. First, we found that treatment of uninjured retinas with a potent agonist of P2RX7 (BzATP) provoked photoreceptor damage and mitotic activation of multipotent progenitors. In CoCl2-injured retinas, blockade of endogenous extracellular ATP activity on P2RX7 caused further neurodegeneration, Müller cell gliosis, progenitor proliferation, and microglia reactivity. P2RX7 inhibition in injured retinas also increased the expression of lin28a and tnfα genes, which are related to multipotent progenitor proliferation. Levels of hif1α, vegf3r, and vegfaa mRNA were enhanced by blockade of P2RX7 immediately after injury, indicating hypoxic like damage and endothelial cell growth and proliferation. Complete depletion of extracellular nucleotides with an apyrase treatment strongly potentiated cell death and progenitor proliferation induced with CoCl2. Blockade of adenosine P1 and A2A receptors (A2AR) had deleterious effects and deregulated normal timing for progenitor and precursor cell proliferation following photoreceptor damage. ATP via P2RX7 and adenosine via A2AR are survival extracellular signals key for retina regeneration in zebrafish.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Wiley-liss, div John Wiley & Sons Inc.
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
A740003
dc.subject
ADENOSINE A2A RECEPTOR
dc.subject
BZATP
dc.subject
MICROGLIA ACTIVATION
dc.subject
P2X7 RECEPTOR
dc.subject
PHOTORECEPTOR DEATH
dc.subject
PROGENITOR PROLIFERATION
dc.subject
RRID: AB_2109952
dc.subject
RRID: AB_2168560
dc.subject
RRID: AB_2315387
dc.subject
RRID: AB_2338000
dc.subject
RRID: AB_2338685
dc.subject
RRID: AB_2338840
dc.subject
RRID: AB_2738589
dc.subject
RRID: AB_514483
dc.subject
RRID: AB_628110
dc.subject.classification
Otras Ciencias Biológicas
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
P2X7 and A2A receptor endogenous activation protects against neuronal death caused by CoCl2-induced photoreceptor toxicity in the zebrafish retina
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2021-09-07T18:55:48Z
dc.journal.volume
528
dc.journal.number
12
dc.journal.pagination
2000-2020
dc.journal.pais
Estados Unidos
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dc.description.fil
Fil: Medrano, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.description.fil
Fil: Pisera Fuster, Antonella. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.description.fil
Fil: Bernabeu, Ramon Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.description.fil
Fil: Faillace, Maria Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.journal.title
Journal Of Comparative Neurology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/cne.24869
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/cne.24869
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