Browsing by Author "Tichauer Calderón, Juan Enrique"

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    A new presentation of the chimeric CYP11B1/CYP11B2 gene with low prevalence of primary aldosteronism and atypical gene segregation pattern
    (Lippincott Williams & Wilkins, 2012) Carvajal Maldonado, Cristian Andrés; Campino Johnson, María del Carmen; Martínez Aguayo, Alejandro Gregorio; Tichauer Calderón, Juan Enrique; Bancalari, Rodrigo; Valdivia, Carolina; Trejo, Pamela; Aglony Imbarack, Marlene Elizabeth; Baudrand Biggs, René Felipe; Lagos Arévalo, Carlos Fernando; Mellado Sagredo, Cecilia Ximena Del Carmen; García Bruce, Hernán Gabriel; Fardella Bello, Carlos Enrique
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    ACIDOSIS INDUCES CHANGES ON SCAVENGER RECEPTORS EXPRESSION PATTERN OF GLIAL CELLS: EFFECT ON CELL ADHESION AND PHAGOCYTOSIS OF ABETA
    (2009) Arroyo Zúñiga, Pablo; Tichauer Calderón, Juan Enrique; Bernhardi Montgomery, Rommy von
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    Inhibition of astroglial hemichannels prevents synaptic transmission decline during spreading depression
    (2024) Tichauer Calderón, Juan Enrique; Lira Mendieta, Matías Sebastián; Cerpa Nebott, Waldo Francisco; Orellana Roca, Juan Andrés; Sáez Carreño, Juan Carlos; Rovegno Echavarría, David Maximiliano
    Spreading depression (SD) is an intriguing phenomenon characterized by massive slow brain depolarizations that affect neurons and glial cells. This phenomenon is repetitive and produces a metabolic overload that increases secondary damage. However, the mechanisms associated with the initiation and propagation of SD are unknown. Multiple lines of evidence indicate that persistent and uncontrolled opening of hemichannels could participate in the pathogenesis and progression of several neurological disorders including acute brain injuries. Here, we explored the contribution of astroglial hemichannels composed of connexin-43 (Cx43) or pannexin-1 (Panx1) to SD evoked by high-K+ stimulation in brain slices. Results Focal high-K+ stimulation rapidly evoked a wave of SD linked to increased activity of the Cx43 and Panx1 hemichannels in the brain cortex, as measured by light transmittance and dye uptake analysis, respectively. The activation of these channels occurs mainly in astrocytes but also in neurons. More importantly, the inhibition of both the Cx43 and Panx1 hemichannels completely prevented high K+-induced SD in the brain cortex. Electrophysiological recordings also revealed that Cx43 and Panx1 hemichannels critically contribute to the SD-induced decrease in synaptic transmission in the brain cortex and hippocampus. Conclusions Targeting Cx43 and Panx1 hemichannels could serve as a new therapeutic strategy to prevent the initiation and propagation of SD in several acute brain injuries.
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    Therapeutic role of interferon-γ in experimental autoimmune encephalomyelitis is mediated through a tolerogenic subset of splenic CD11b+ myeloid cells
    (2024) Arellano, Gabriel; Acuña, Eric; Loda, Eileah; Moore, Lindsay; Tichauer Calderón, Juan Enrique; Castillo, Cristian; Vergara, Fabian; Burgos Cañete, Paula Isabel; Peñaloza-MacMaster, Pablo; Miller, Stephen D.; Naves, Rodrigo
    Cumulative evidence has established that Interferon (IFN)-γ has both pathogenic and protective roles in Multiple Sclerosis and the animal model, Experimental Autoimmune Encephalomyelitis (EAE). However, the underlying mechanisms to the beneficial effects of IFN-γ are not well understood. In this study, we found that IFN-γ exerts therapeutic effects on chronic, relapsing-remitting, and chronic progressive EAE models. The frequency of regulatory T (Treg) cells in spinal cords from chronic EAE mice treated with IFN-γ was significantly increased with no effect on Th1 and Th17 cells. Consistently, depletion of FOXP3-expressing cells blocked the protective effects of IFN-γ, indicating that the therapeutic effect of IFN-γ depends on the presence of Treg cells. However, IFN-γ did not trigger direct in vitro differentiation of Treg cells. In vivo administration of blocking antibodies against either interleukin (IL)-10, transforming growth factor (TGF)-β or program death (PD)-1, revealed that the protective effects of IFN-γ in EAE were also dependent on TGF-β and PD-1, but not on IL-10, suggesting that IFN-γ might have an indirect role on Treg cells acting through antigen-presenting cells. Indeed, IFN-γ treatment increased the frequency of a subset of splenic CD11b+ myeloid cells expressing TGF-β-Latency Associated Peptide (LAP) and program death ligand 1 (PD-L1) in a signal transducer and activator of transcription (STAT)-1-dependent manner. Furthermore, splenic CD11b+ cells from EAE mice preconditioned in vitro with IFN-γ and myelin oligodendrocyte glycoprotein (MOG) peptide exhibited a tolerogenic phenotype with the capability to induce conversion of naïve CD4+ T cells mediated by secretion of TGF-β. Remarkably, adoptive transfer of splenic CD11b+ cells from IFN-γ-treated EAE mice into untreated recipient mice ameliorated clinical symptoms of EAE and limited central nervous system infiltration of mononuclear cells and effector helper T cells. These results reveal a novel cellular and molecular mechanism