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Oxygen and HIF1α-dependent SDF1 expression in primary astrocytes.
Pietrucha, Andreas; Serdar, Meray; Bendix, Ivo; Endesfelder, Stefanie; Brinke, Elena Auf dem; Urkola, Ane; Bührer, Christoph; Schmitz, Thomas; Scheuer, Till.
Afiliación
  • Pietrucha A; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Serdar M; Department of Pediatrics I, Neonatology and Experimental perinatal Neurosciences, Centre for Translational and Behavioral Sciences (C-TNBS), University Hospital Essen, University Duisburg-Essen, Essen, Germany.
  • Bendix I; Department of Pediatrics I, Neonatology and Experimental perinatal Neurosciences, Centre for Translational and Behavioral Sciences (C-TNBS), University Hospital Essen, University Duisburg-Essen, Essen, Germany.
  • Endesfelder S; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Brinke EAD; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Urkola A; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Bührer C; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Schmitz T; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
  • Scheuer T; Department of Neonatology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Dev Neurobiol ; 84(3): 113-127, 2024 Jul.
Article en En | MEDLINE | ID: mdl-38544386
ABSTRACT
In the naturally hypoxic in utero fetal environment of preterm infants, oxygen and oxygen-sensitive signaling pathways play an important role in brain development, with hypoxia-inducible factor-1α (HIF1α) being an important regulator. Early exposure to nonphysiological high oxygen concentrations by birth in room can induce HIF1α degradation and may affect neuronal and glial development. This involves the dysregulation of astroglial maturation and function, which in turn might contribute to oxygen-induced brain injury. In this study, we investigated the effects of early high oxygen exposure on astroglial maturation and, specifically, on astroglial stromal cell-derived factor 1 (SDF1) expression in vivo and in vitro. In our neonatal mouse model of hyperoxia preterm birth brain injury in vivo, high oxygen exposure affected astroglial development and cortical SDF1 expression. These results were further supported by reduced Sdf1 expression, impaired proliferation, decreased total cell number, and altered expression of astroglial markers in astrocytes in primary cultures grown under high oxygen conditions. Moreover, to mimic the naturally hypoxic in utero fetal environment, astroglial Sdf1 expression was increased after low oxygen exposure in vitro, which appears to be regulated by HIF1α activity. Additionally, the knockdown of Hif1α revealed HIF1α-dependent Sdf1 expression in vitro. Our results indicate HIF1α and oxygen-dependent chemokine expression in primary astrocytes and highlight the importance of oxygen conditions for brain development.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxígeno / Astrocitos / Subunidad alfa del Factor 1 Inducible por Hipoxia / Quimiocina CXCL12 / Animales Recién Nacidos Límite: Animals Idioma: En Revista: Dev Neurobiol Asunto de la revista: BIOLOGIA / NEUROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Oxígeno / Astrocitos / Subunidad alfa del Factor 1 Inducible por Hipoxia / Quimiocina CXCL12 / Animales Recién Nacidos Límite: Animals Idioma: En Revista: Dev Neurobiol Asunto de la revista: BIOLOGIA / NEUROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos