Altered PLCβ/IP3/Ca2+ Signaling Pathway Activated by GPRCs in Olfactory Neuronal Precursor Cells Derived from Patients Diagnosed with Schizophrenia

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dc.contributor.affiliationDepartamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City 04510, CP, Mexico.
dc.contributor.emailjaimezruth@hotmail.com
dc.creatorSánchez-Florentino, Zuly A.
dc.creatorRomero-Martínez, Bianca S.
dc.creatorFlores-Soto, Edgar
dc.creatorMontaño, Luis M.
dc.creatorSommer, Bettina
dc.creatorValdés-Tovar, Marcela
dc.creatorArgueta, Jesús
dc.creatorCalixto, Eduardo
dc.creatorAquino-Gálvez, Arnoldo
dc.creatorCastillejos-López, Manuel
dc.creatorSerrano, Héctor
dc.creatorGomez-Verjan, Juan C.
dc.creatorLópez-Riquelme, Germán O.
dc.creatorBenítez-King, Gloria A.
dc.creatorJaimez, Ruth
dc.creatorSolís-Chagoyán, Héctor
dc.date2024
dc.date.accessioned2026-06-15T19:41:23Z
dc.date.issued2024
dc.date.published2024
dc.descriptionSchizophrenia (SZ) is a multifactorial chronic psychiatric disorder with a worldwide prevalence of 1%. Altered expression of PLCβ occurs in SZ patients, suggesting alterations in the PLCβ/IP3/Ca2+ signaling pathway. This cascade regulates critical cellular processes in all cell types, including the neuronal lineage; however, there is scarce evidence regarding the functionality of this transduction signaling in neuronal cells derived from SZ patients. Objective: We evaluated the functionality of the PLCβ/IP3/Ca2+ pathway in olfactory neuronal precursor cells (hONPCs) obtained from SZ patients. Methods: Cryopreserved hONPCs isolated from SZ patients and healthy subjects (HS) were thawed. The cellular types in subcultures were corroborated by immunodetection of the multipotency and lineage markers SOX-2, Musashi-1, nestin, and β-III tubulin. The PLCβ/IP3/Ca2+ pathway was activated by GPCR (Gq) ligands (ATP, UTP, serotonin, and epinephrine). In addition, PLCβ and IP3R were directly stimulated by perfusing cells with the activators m-3M3FBS and ADA, respectively. Cytosolic Ca2+ was measured by microfluorometry and by Ca2+ imaging. The amount and subcellular distribution of the PLCβ1 and PLCβ3 isoforms were evaluated by confocal immunofluorescence. IP3 concentration was measured by ELISA. Results: The results show that the increase of cytosolic Ca2+ triggered by GPCR ligands or directly through either PLCβ or IP3R activation was significantly lower in SZ-derived hONPCs, regarding HS-derived cells. Moreover, the relative amount of the PLCβ1 and PLCβ3 isoforms and IP3 production stimulated with m-3M3FBS were reduced in SZ-derived cells. Conclusions: Our results suggest an overall functional impairment in the PLCβ/IP3/Ca2+ signaling pathway in SZ-derived hONPCs.
dc.formatPDF
dc.identifierOE14IC2025
dc.identifier.doi10.3390/biomedicines12102343
dc.identifier.eissn2227-9059
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/101
dc.identifier.urihttps://doi.org/10.3390/biomedicines12102343
dc.language.isoeng
dc.publisherMDPI
dc.relation15;12(10):2343
dc.relation.jnabreviadoBiomedicines
dc.relation.journalBiomedicines
dc.rightsAcceso Cerrado
dc.subject.kwIP3
dc.subject.kwPLCβ
dc.subject.kwCalcium signaling
dc.subject.kwHuman olfactory neuronal stem cells
dc.subject.kwschizophrenia.
dc.titleAltered PLCβ/IP3/Ca2+ Signaling Pathway Activated by GPRCs in Olfactory Neuronal Precursor Cells Derived from Patients Diagnosed with Schizophrenia
dc.typeArticulo

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