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dc.contributor.author
Netti, Vanina Alejandra
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Pizzoni, Alejandro
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Peréz Domínguez, Martha
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Ford, Paula
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Pasantes Morales, Herminia
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Ramos Mandujano, Gerardo
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Capurro, Claudia Graciela
dc.date.available
2019-11-08T18:56:55Z
dc.date.issued
2018-09
dc.identifier.citation
Netti, Vanina Alejandra; Pizzoni, Alejandro; Peréz Domínguez, Martha; Ford, Paula; Pasantes Morales, Herminia; et al.; Release of taurine and glutamate contributes to cell volume regulation in human retinal Müller cells: Differences in modulation by calcium; American Physiological Society; Journal of Neurophysiology; 120; 3; 9-2018; 973-984
dc.identifier.issn
0022-3077
dc.identifier.uri
http://hdl.handle.net/11336/88380
dc.description.abstract
Neuronal activity in the retina generates osmotic gradients that lead to Müller cell swelling, followed by a regulatory volume decrease (RVD) response, partially due to the isoosmotic efflux of KCl and water. However, our previous studies in a human Müller cell line (MIO-M1) demonstrated that an important fraction of RVD may also involve the efflux of organic solutes. We also showed that RVD depends on the swelling-induced Ca 2+ release from intracellular stores. Here we investigate the contribution of taurine (Tau) and glutamate (Glu), the most relevant amino acids in Müller cells, to RVD through the volume-regulated anion channel (VRAC), as well as their Ca 2+ dependency in MIO-M1 cells. Swelling-induced [ 3 H]Tau/ [ 3 H]Glu release was assessed by radiotracer assays and cell volume by fluorescence videomicroscopy. Results showed that cells exhibited an osmosensitive efflux of [ 3 H]Tau and [ 3 H]Glu (Tau > Glu) blunted by VRAC inhibitors 4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)-oxybutyric acid and carbenoxolone reducing RVD. Only [ 3 H]Tau efflux was mainly dependent on Ca 2+ release from intracellular stores. RVD was unaffected in a Ca 2+ -free medium, probably due to Ca 2+ -independent Tau and Glu release, but was reduced by chelating intracellular Ca 2+ . The inhibition of phosphatidylinositol-3-kinase reduced [ 3 H]Glu efflux but also the Ca 2+ -insensitive [ 3 H]Tau fraction and decreased RVD, providing evidence of the relevance of this Ca 2+ -independent pathway. We propose that VRAC-mediated Tau and Glu release has a relevant role in RVD in Müller cells. The observed disparities in Ca 2+ influence on amino acid release suggest the presence of VRAC isoforms that may differ in substrate selectivity and regulatory mechanisms, with important implications for retinal physiology. NEW & NOTEWORTHY The mechanisms for cell volume regulation in retinal Müller cells are still unknown. We show that swelling-induced taurine and glutamate release mediated by the volume-regulated anion channel (VRAC) largely contributes the to the regu- latory volume decrease response in a human Müller cell line. Interestingly, the hypotonic-induced efflux of these amino acids exhibits disparities in Ca 2+ -dependent and-independent regulatory mechanisms, which strongly suggests that Müller cells may express different VRAC heteromers formed by the recently discovered leu-cine-rich repeat containing 8 (LRRC8) proteins.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
CELL VOLUME REGULATION
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GLUTAMATE
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HUMAN MÜLLER CELLS
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TAURINE
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VOLUME-REGULATED ANION CHANNEL
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Otras Ciencias Biológicas
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
Release of taurine and glutamate contributes to cell volume regulation in human retinal Müller cells: Differences in modulation by calcium
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-16T18:28:39Z
dc.journal.volume
120
dc.journal.number
3
dc.journal.pagination
973-984
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Bethesda
dc.description.fil
Fil: Netti, Vanina Alejandra. 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: Pizzoni, Alejandro. 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
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Fil: Peréz Domínguez, Martha. Universidad Nacional Autónoma de México; México
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Fil: Ford, 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.description.fil
Fil: Pasantes Morales, Herminia. Universidad Nacional Autónoma de México; México
dc.description.fil
Fil: Ramos Mandujano, Gerardo. Universidad Nacional Autónoma de México; México
dc.description.fil
Fil: Capurro, Claudia Graciela. 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 Neurophysiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/10.1152/jn.00725.2017
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/jn.00725.2017
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