dc.creatorMoyano, Alejandro Jose
dc.creatorRacca, Ana Cristina
dc.creatorSoria, Ramiro Gaston
dc.creatorSaka, Hector Alex
dc.creatorAndreoli, Veronica
dc.creatorSmania, Andrea
dc.creatorSola, Claudia del Valle
dc.creatorBocco, Jose Luis
dc.date.accessioned2020-01-24T22:45:43Z
dc.date.accessioned2022-10-14T21:30:33Z
dc.date.available2020-01-24T22:45:43Z
dc.date.available2022-10-14T21:30:33Z
dc.date.created2020-01-24T22:45:43Z
dc.date.issued2018-05
dc.identifierMoyano, Alejandro Jose; Racca, Ana Cristina; Soria, Ramiro Gaston; Saka, Hector Alex; Andreoli, Veronica; et al.; c-Jun Proto-Oncoprotein Plays a Protective Role in Lung Epithelial Cells Exposed to Staphylococcal α-toxin; Frontiers Media SA; Frontiers in Cellular and Infection Microbiology; 8; 5-2018; 1-9
dc.identifier2235-2988
dc.identifierhttp://hdl.handle.net/11336/95816
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/4308894
dc.description.abstractc-Jun is a member of the early mammalian transcriptional regulators belonging to the AP-1 family, which participates in a wide range of cellular processes such as proliferation, apoptosis, tumorigenesis, and differentiation. Despite its established role in cell survival upon stress, its participation in the stress response induced by bacterial infections has been poorly investigated. To study the potential role of c-Jun in this context we choose the widely studied α-toxin produced by Staphylococcus aureus, a pore-forming toxin that is a critical virulence factor in the pathogenesis of these bacteria. We analyzed the effect of α-toxin treatment in the activation, expression, and protein levels of c-Jun in A549 lung epithelial cells. Furthermore, we explored the role of c-Jun in the cellular fate after exposure to α-toxin. Our results show that staphylococcal α-toxin per se is able to activate c-Jun by inducing phosphorylation of its Serine 73 residue. Silencing of the JNK (c-Jun N-terminal Kinase) signaling pathway abrogated most of this activation. On the contrary, silencing of the ERK (Extracellular Signal-Regulated Kinase) pathway exacerbated this response. Intriguingly, while the exposure to α-toxin induced a marked increase in the levels of c-Jun transcripts, c-Jun protein levels noticeably decreased in the same time-frame as a consequence of active proteolytic degradation through the proteasome-dependent pathway. In addition, we established that c-Jun promoted cell survival when cells were challenged with α-toxin. Similarly, c-Jun phosphorylation was also induced in cells upon intoxication with the cytolysin produced by Vibrio cholerae in a JNK-dependent manner, suggesting that c-Jun-JNK axis would be a conserved responsive cellular pathway to pore-forming toxins. This study contributes to understanding the role of the multifaceted c-Jun proto-oncoprotein in cell response to bacterial pore-forming toxins, positioning it as a relevant component of the complex early machinery mounted to deal with staphylococcal infections.
dc.languageeng
dc.publisherFrontiers Media SA
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/article/10.3389/fcimb.2018.00170/full
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.3389/fcimb.2018.00170
dc.rightshttps://creativecommons.org/licenses/by/2.5/ar/
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectA-HEMOLYSIN
dc.subjectA-TOXIN
dc.subjectBACTERIAL PORE-FORMING TOXINS
dc.subjectC-JUN
dc.subjectSTAPHYLOCOCCUS AUREUS
dc.titlec-Jun Proto-Oncoprotein Plays a Protective Role in Lung Epithelial Cells Exposed to Staphylococcal α-toxin
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:ar-repo/semantics/artículo
dc.typeinfo:eu-repo/semantics/publishedVersion


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