TNF-α Plus IL-1β Induces Opposite Regulation of Cx43 Hemichannels and Gap Junctions in Mesangial Cells through a RhoA/ROCK-Dependent Pathway

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dc.catalogadorgjm
dc.contributor.authorLucero, Claudia M.
dc.contributor.authorMarambio-Ruiz, Lucas
dc.contributor.authorBalmazabal, Javiera
dc.contributor.authorPrieto Villalobos, Juan Carlos
dc.contributor.authorLeon, Marcelo
dc.contributor.authorFernandez, Paola
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorVelarde Aliaga, María Victoria
dc.contributor.authorSaez, Juan C.
dc.contributor.authorGomez, Gonzalo, I
dc.date.accessioned2024-10-16T16:33:52Z
dc.date.available2024-10-16T16:33:52Z
dc.date.issued2022
dc.description.abstractConnexin 43 (Cx43) is expressed in kidney tissue where it forms hemichannels and gap junction channels. However, the possible functional relationship between these membrane channels and their role in damaged renal cells remains unknown. Here, analysis of ethidium uptake and thiobarbituric acid reactive species revealed that treatment with TNF-alpha plus IL-1 beta increases Cx43 hemichannel activity and oxidative stress in MES-13 cells (a cell line derived from mesangial cells), and in primary mesangial cells. The latter was also accompanied by a reduction in gap junctional communication, whereas Western blotting assays showed a progressive increase in phosphorylated MYPT (a target of RhoA/ROCK) and Cx43 upon TNF-alpha/IL-1 beta treatment. Additionally, inhibition of RhoA/ROCK strongly antagonized the TNF-alpha/IL-1 beta-induced activation of Cx43 hemichannels and reduction in gap junctional coupling. We propose that activation of Cx43 hemichannels and inhibition of cell-cell coupling during pro-inflammatory conditions could contribute to oxidative stress and damage of mesangial cells via the RhoA/ROCK pathway.
dc.fechaingreso.objetodigital2024-10-16
dc.format.extent20 páginas
dc.fuente.origenORCID
dc.identifier.doi10.3390/ijms231710097
dc.identifier.eissn1422-0067
dc.identifier.urihttp://doi.org/10.3390/ijms231710097
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88266
dc.identifier.wosidWOS:000851150600001
dc.information.autorucEscuela de Medicina; Prieto Villalobos, Juan Carlos; S/I; 1071673
dc.information.autorucEscuela de Medicina; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.information.autorucFacultad de Ciencias Biológicas; Velarde Aliaga, María Victoria; S/I; 55362
dc.issue.numero17
dc.language.isoen
dc.nota.accesocontenido completo
dc.revistaInternational Journal of Molecular Sciences
dc.rightsacceso abierto
dc.rights.licenseCC BY 4.0 Attribution 4.0 International Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectConnexin hemichannel
dc.subjectGap junction
dc.subjectOxidative stress
dc.subjectInflammatory receptors
dc.subjectFasudil
dc.subjectY-27632
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleTNF-α Plus IL-1β Induces Opposite Regulation of Cx43 Hemichannels and Gap Junctions in Mesangial Cells through a RhoA/ROCK-Dependent Pathway
dc.typeartículo
dc.volumen23
sipa.codpersvinculados1071673
sipa.codpersvinculados126007
sipa.codpersvinculados55362
sipa.trazabilidadORCID;2024-10-14
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