Activation of Pannexin-1 channels causes cell dysfunction and damage in mesangial cells derived from angiotensin II-exposed mice

Simple item page
dc.article.number1387234
dc.catalogadorvdr
dc.contributor.authorLucero, Claudia M.
dc.contributor.authorNavarro, Laura
dc.contributor.authorBarros-Osorio, Cristián
dc.contributor.authorCáceres-Conejeros, Patricio
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorGómez, Gonzalo I.
dc.date.accessioned2024-10-15T13:50:52Z
dc.date.available2024-10-15T13:50:52Z
dc.date.issued2024
dc.description.abstractCopyright © 2024 Lucero, Navarro, Barros-Osorio, Cáceres-Conejeros, Orellana and Gómez.Chronic kidney disease (CKD) is a prevalent health concern associated with various pathological conditions, including hypertensive nephropathy. Mesangial cells are crucial in maintaining glomerular function, yet their involvement in CKD pathogenesis remains poorly understood. Recent evidence indicates that overactivation of Pannexin-1 (Panx1) channels could contribute to the pathogenesis and progression of various diseases. Although Panx1 is expressed in the kidney, its contribution to the dysfunction of renal cells during pathological conditions remains to be elucidated. This study aimed to investigate the impact of Panx1 channels on mesangial cell function in the context of hypertensive nephropathy. Using an Ang II-infused mouse model and primary mesangial cell cultures, we demonstrated that in vivo exposure to Ang II sensitizes cultured mesangial cells to show increased alterations when they are subjected to subsequent in vitro exposure to Ang II. Particularly, mesangial cell cultures treated with Ang II showed elevated activity of Panx1 channels and increased release of ATP. The latter was associated with enhanced basal intracellular Ca2+ ([Ca2+]i) and increased ATP-mediated [Ca2+]i responses. These effects were accompanied by increased lipid peroxidation and reduced cell viability. Crucially, all the adverse impacts evoked by Ang II were prevented by the blockade of Panx1 channels, underscoring their critical role in mediating cellular dysfunction in mesangial cells. By elucidating the mechanisms by which Ang II negatively impacts mesangial cell function, this study provides valuable insights into the pathogenesis of renal damage in hypertensive nephropathy.
dc.description.funderAgencia Nacional de Investigación y Desarrollo
dc.description.funderFondo Nacional de Desarrollo Científico y Tecnológico
dc.fechaingreso.objetodigital2024-10-15
dc.fuente.origenSCOPUS
dc.fuente.origenORCID
dc.identifier.doi10.3389/fcell.2024.1387234
dc.identifier.issn2296-634X
dc.identifier.scopusidSCOPUS_ID:85191051699
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88230
dc.identifier.urihttps://doi.org/10.3389/fcell.2024.1387234
dc.identifier.wosidWOS:001206978800001
dc.information.autorucFacultad de Ciencias Biológicas; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.language.isoen
dc.nota.accesocontenido completo
dc.publisherFrontiers Media SA
dc.revistaFrontiers in Cell and Developmental Biology
dc.rightsacceso abierto
dc.rights.licenseCC BY 4.0 Attribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectATP
dc.subjectHypertensive nephropathy
dc.subjectInflammation
dc.subjectIntracellular Ca2+
dc.subjectPanx1
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleActivation of Pannexin-1 channels causes cell dysfunction and damage in mesangial cells derived from angiotensin II-exposed mice
dc.typeartículo
dc.volumen12
sipa.codpersvinculados126007
sipa.trazabilidadSCOPUS;2024-05-05
sipa.trazabilidadORCID;2024-10-14
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
fcell-12-1387234.pdf
Size:
2.45 MB
Format:
Adobe Portable Document Format
Description:
Download
Collections
Artículos de revistas