Interleukin 3 Inhibits Glutamate-Cytotoxicity in Neuroblastoma Cell Line

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dc.catalogadorjwg
dc.contributor.authorMatus, Verónica
dc.contributor.authorCastro-Guarda, Marcos
dc.contributor.authorCarcamo-Fierro, Joaquin
dc.contributor.authorMorera Galleguillos Francisco Javier
dc.contributor.authorZambrano, Angara
dc.date.accessioned2024-04-04T15:02:58Z
dc.date.available2024-04-04T15:02:58Z
dc.date.issued2024
dc.description.abstractInterleukin 3 (IL-3) is a well-known pleiotropic cytokine that regulates the proliferation and differentiation of hematopoietic progenitor cells, triggering classical signaling pathways such as JAK/STAT, Ras/MAPK, and PI3K/Akt to carry out its functions. Interestingly, the IL-3 receptor is also expressed in non-hematopoietic cells, playing a crucial role in cell survival. Our previous research demonstrated the expression of the IL-3 receptor in neuron cells and its protective role in neurodegeneration. Glutamate, a principal neurotransmitter in the central nervous system, can induce cellular stress and lead to neurotoxicity when its extracellular concentrations surpass normal levels. This excessive glutamate presence is frequently observed in various neurological diseases. In this study, we uncover the protective role of IL-3 as an inhibitor of glutamate-induced cell death, analyzing the cytokine's signaling pathways during its protective effect. Specifically, we examined the relevance of JAK/STAT, Ras/MAPK, and PI3 K signaling pathways in the molecular mechanism triggered by IL-3. Our results show that the inhibition of JAK, ERK, and PI3 K signaling pathways, using pharmacological inhibitors, effectively blocked IL-3's protective role against glutamate-induced cell death. Additionally, our findings suggest that Bcl-2 and Bax proteins may be involved in the molecular mechanism triggered by IL-3. Our investigation into IL-3's ability to protect neuronal cells from glutamate-induced damage offers a promising therapeutic avenue with potential clinical implications for several neurological diseases characterized by glutamate neurotoxicity.
dc.description.funderPrograma de Insercion Academica, Vicerrectoria Academica, P Universidad Catlica de Chile .
dc.fechaingreso.objetodigital2024-08-30
dc.fuente.origenORCID
dc.identifier.doi10.1007/s11064-024-04123-x
dc.identifier.eissn1573-6903
dc.identifier.issn0364-3190
dc.identifier.urihttps://doi.org/10.1007/s11064-024-04123-x
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/84947
dc.identifier.wosidWOS:001188091800002
dc.information.autorucFacultad de Ciencias Biológicas; Morera Galleguillos Francisco Javier; S/l; 17437
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final1386
dc.pagina.inicio1373
dc.publisherSpringer
dc.revistaNeurochemical Research
dc.rightsacceso restringido
dc.subjectIL-3
dc.subjectGlutamate cytotoxicity
dc.subjectNeuroprotection
dc.subjectApoptotic cell death
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInterleukin 3 Inhibits Glutamate-Cytotoxicity in Neuroblastoma Cell Line
dc.typeartículo
dc.volumen49
sipa.codpersvinculados17437
sipa.trazabilidadORCID;2024-04-01
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