Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells
Unconjugated bilirubin (UCB) encephalopathy is a predominantly early life condition resulting from the impairment of several cellular functions in the brain of severely jaundiced infants. However, only few data exist on the age-dependent effects of UCB and their association with increased vulnerabil...
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doaj-f3759531313a4a208a8b88a5ae35f0802021-03-20T04:51:09ZengElsevierNeurobiology of Disease1095-953X2005-11-01202199206Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cellsAna S. Falcão0Adelaide Fernandes1Maria A. Brito2Rui F.M. Silva3Dora Brites4Centro de Patogénese Molecular (UBMBE), Faculdade de Farmácia, University of Lisbon, Av. Forças Armadas, 1600-083 Lisboa, PortugalCentro de Patogénese Molecular (UBMBE), Faculdade de Farmácia, University of Lisbon, Av. Forças Armadas, 1600-083 Lisboa, PortugalCentro de Patogénese Molecular (UBMBE), Faculdade de Farmácia, University of Lisbon, Av. Forças Armadas, 1600-083 Lisboa, PortugalCentro de Patogénese Molecular (UBMBE), Faculdade de Farmácia, University of Lisbon, Av. Forças Armadas, 1600-083 Lisboa, PortugalCorresponding author. Fax: +351 21 7946491.; Centro de Patogénese Molecular (UBMBE), Faculdade de Farmácia, University of Lisbon, Av. Forças Armadas, 1600-083 Lisboa, PortugalUnconjugated bilirubin (UCB) encephalopathy is a predominantly early life condition resulting from the impairment of several cellular functions in the brain of severely jaundiced infants. However, only few data exist on the age-dependent effects of UCB and their association with increased vulnerability of premature newborns, particularly in a sepsis condition. We investigated cell death, glutamate efflux, and inflammatory cytokine dynamics after exposure of astrocytes at different stages of differentiation to clinically relevant concentrations of UCB and/or lipopolysaccharide (LPS). Younger astrocytes were more prone to UCB-induced cell death, glutamate efflux, and inflammatory response than older ones. Furthermore, in immature cells, LPS exacerbated UCB effects, such as cell death by necrosis. These findings provide a basis for the increased susceptibility of premature newborns to UCB deleterious effects, namely when associated with sepsis, and underline how crucial the course of cell maturation can be to UCB encephalopathy during moderate to severe neonatal jaundice.http://www.sciencedirect.com/science/article/pii/S096999610500077XAstrocytesDevelopmentCell deathGlutamate releaseLipopolysaccharide (LPS)Cytokines |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ana S. Falcão Adelaide Fernandes Maria A. Brito Rui F.M. Silva Dora Brites |
spellingShingle |
Ana S. Falcão Adelaide Fernandes Maria A. Brito Rui F.M. Silva Dora Brites Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells Neurobiology of Disease Astrocytes Development Cell death Glutamate release Lipopolysaccharide (LPS) Cytokines |
author_facet |
Ana S. Falcão Adelaide Fernandes Maria A. Brito Rui F.M. Silva Dora Brites |
author_sort |
Ana S. Falcão |
title |
Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
title_short |
Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
title_full |
Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
title_fullStr |
Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
title_full_unstemmed |
Bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
title_sort |
bilirubin-induced inflammatory response, glutamate release, and cell death in rat cortical astrocytes are enhanced in younger cells |
publisher |
Elsevier |
series |
Neurobiology of Disease |
issn |
1095-953X |
publishDate |
2005-11-01 |
description |
Unconjugated bilirubin (UCB) encephalopathy is a predominantly early life condition resulting from the impairment of several cellular functions in the brain of severely jaundiced infants. However, only few data exist on the age-dependent effects of UCB and their association with increased vulnerability of premature newborns, particularly in a sepsis condition. We investigated cell death, glutamate efflux, and inflammatory cytokine dynamics after exposure of astrocytes at different stages of differentiation to clinically relevant concentrations of UCB and/or lipopolysaccharide (LPS). Younger astrocytes were more prone to UCB-induced cell death, glutamate efflux, and inflammatory response than older ones. Furthermore, in immature cells, LPS exacerbated UCB effects, such as cell death by necrosis. These findings provide a basis for the increased susceptibility of premature newborns to UCB deleterious effects, namely when associated with sepsis, and underline how crucial the course of cell maturation can be to UCB encephalopathy during moderate to severe neonatal jaundice. |
topic |
Astrocytes Development Cell death Glutamate release Lipopolysaccharide (LPS) Cytokines |
url |
http://www.sciencedirect.com/science/article/pii/S096999610500077X |
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