Control of astrocytic Ca2+ signaling by nitric oxide-dependent S-nitrosylation of Ca2+ homeostasis modulator 1 channels

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dc.article.number19
dc.catalogadorpva
dc.contributor.authorPuebla Catalán, Mariela del Carmen
dc.contributor.authorMuñoz Camus, Manuel Francisco
dc.contributor.authorLillo Gallardo, Mauricio Alejandro
dc.contributor.authorContreras, Jorge E.
dc.contributor.authorFigueroa, Xavier
dc.date.accessioned2024-05-07T16:11:53Z
dc.date.available2024-05-07T16:11:53Z
dc.date.issued2024
dc.date.updated2024-05-05T00:05:13Z
dc.description.abstractBackground Astrocytes Ca2+ signaling play a central role in the modulation of neuronal function. Activation of metabotropic glutamate receptors (mGluR) by glutamate released during an increase in synaptic activity triggers coordinated Ca2+ signals in astrocytes. Importantly, astrocytes express the Ca2+-dependent nitric oxide (NO)-synthetizing enzymes eNOS and nNOS, which might contribute to the Ca2+ signals by triggering Ca2+ influx or ATP release through the activation of connexin 43 (Cx43) hemichannels, pannexin-1 (Panx-1) channels or Ca2+ homeostasis modulator 1 (CALHM1) channels. Hence, we aim to evaluate the participation of NO in the astrocytic Ca2+ signaling initiated by stimulation of mGluR in primary cultures of astrocytes from rat brain cortex. Results: Astrocytes were stimulated with glutamate or t-ACPD and NO-dependent changes in [Ca2+]i and ATP release were evaluated. In addition, the activity of Cx43 hemichannels, Panx-1 channels and CALHM1 channels was also analyzed. The expression of Cx43, Panx-1 and CALHM1 in astrocytes was confirmed by immunofluorescence analysis and both glutamate and t-ACPD induced NO-mediated activation of CALHM1 channels via direct S-nitrosylation, which was further confirmed by assessing CALHM1-mediated current using the two-electrode voltage clamp technique in Xenopus oocytes. Pharmacological blockade or siRNA-mediated inhibition of CALHM1 expression revealed that the opening of these channels provides a pathway for ATP release and the subsequent purinergic receptor-dependent activation of Cx43 hemichannels and Panx-1 channels, which further contributes to the astrocytic Ca2+ signaling. Conclusions Our findings demonstrate that activation of CALHM1 channels through NO-mediated S-nitrosylation in astrocytes in vitro is critical for the generation of glutamate-initiated astrocytic Ca2+ signaling.
dc.fechaingreso.objetodigital2024-05-05
dc.fuente.origenAutoarchivo
dc.identifier.citationBiological Research. 2024 Apr 30;57(1):19
dc.identifier.urihttps://doi.org/10.1186/s40659-024-00503-3
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/85480
dc.information.autorucFacultad de Ciencias Biológicas; Puebla Catalán, Mariela del Carmen; S/I; 217998
dc.information.autorucFacultad de Ciencias Biológicas; Muñoz Camus, Manuel Francisco; S/I; 195470
dc.information.autorucFacultad de Ciencias Biológicas; Lillo Gallardo, Mauricio Alejandro; S/I; 156079
dc.information.autorucFacultad de Ciencias Biológicas; Contreras, Jorge E.; S/I; 96418
dc.information.autorucFacultad de Ciencias Biológicas; Figueroa, Xavier; 0000-0001-9656-9100; 1437
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final19
dc.pagina.inicio1
dc.revistaBiological Research
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.rights.licenseAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectNitric oxide
dc.subjectAstrocytes
dc.subjectCa2+ signaling
dc.subjectCALHM1 channels
dc.subjectATP release
dc.subjectConnexin 43 hemichannels
dc.subjectPannexin-1 channels
dc.subject.ddc570
dc.subject.deweyBiologíaes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleControl of astrocytic Ca2+ signaling by nitric oxide-dependent S-nitrosylation of Ca2+ homeostasis modulator 1 channels
dc.typeartículo
dc.volumen57
sipa.codpersvinculados217998
sipa.codpersvinculados195470
sipa.codpersvinculados1437
sipa.codpersvinculados156079
sipa.codpersvinculados96418
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