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Microglia toxicity in preterm brain injury

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Microglia toxicity in preterm brain injury. / Baburamani, Ana A.; Supramaniam, Veena G.; Hagberg, Henrik; Mallard, Carina.

In: Reproductive Toxicology, Vol. 48, 09.2014, p. 106-112.

Research output: Contribution to journalArticle

Harvard

Baburamani, AA, Supramaniam, VG, Hagberg, H & Mallard, C 2014, 'Microglia toxicity in preterm brain injury', Reproductive Toxicology, vol. 48, pp. 106-112. https://doi.org/10.1016/j.reprotox.2014.04.002

APA

Baburamani, A. A., Supramaniam, V. G., Hagberg, H., & Mallard, C. (2014). Microglia toxicity in preterm brain injury. Reproductive Toxicology, 48, 106-112. https://doi.org/10.1016/j.reprotox.2014.04.002

Vancouver

Baburamani AA, Supramaniam VG, Hagberg H, Mallard C. Microglia toxicity in preterm brain injury. Reproductive Toxicology. 2014 Sep;48:106-112. https://doi.org/10.1016/j.reprotox.2014.04.002

Author

Baburamani, Ana A. ; Supramaniam, Veena G. ; Hagberg, Henrik ; Mallard, Carina. / Microglia toxicity in preterm brain injury. In: Reproductive Toxicology. 2014 ; Vol. 48. pp. 106-112.

Bibtex Download

@article{a71ff1b3bd484245a9f9519304203d80,
title = "Microglia toxicity in preterm brain injury",
abstract = "Microglia are the resident phagocytic cells of the central nervous system. During brain development they are also imperative for apoptosis of excessive neurons, synaptic pruning, phagocytosis of debris and maintaining brain homeostasis. Brain damage results in a fast and dynamic microglia reaction, which can influence the extent and distribution of subsequent neuronal dysfunction. As a consequence, microglia responses can promote tissue protection and repair following brain injury, or become detrimental for the tissue integrity and functionality. In this review, we will describe microglia responses in the human developing brain in association with injury, with particular focus on the preterm infant. We also explore microglia responses and mechanisms of microglia toxicity in animal models of preterm white matter injury and in vitro primary microglia cell culture experiments.",
keywords = "Perinatal brain injury, Neuroinflammation, WHITE-MATTER INJURY, TUMOR-NECROSIS-FACTOR, BACTERIAL-ENDOTOXIN SENSITIZES, ORGANOTYPIC SLICE CULTURES, NITRIC-OXIDE SYNTHASE, CELLS IN-VITRO, ACTIVATED MICROGLIA, PERIVENTRICULAR LEUKOMALACIA, FETAL SHEEP, GLUTAMATE-RECEPTOR",
author = "Baburamani, {Ana A.} and Supramaniam, {Veena G.} and Henrik Hagberg and Carina Mallard",
year = "2014",
month = sep,
doi = "10.1016/j.reprotox.2014.04.002",
language = "English",
volume = "48",
pages = "106--112",
journal = "Reproductive Toxicology",
issn = "0890-6238",
publisher = "Elsevier Inc.",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Microglia toxicity in preterm brain injury

AU - Baburamani, Ana A.

AU - Supramaniam, Veena G.

AU - Hagberg, Henrik

AU - Mallard, Carina

PY - 2014/9

Y1 - 2014/9

N2 - Microglia are the resident phagocytic cells of the central nervous system. During brain development they are also imperative for apoptosis of excessive neurons, synaptic pruning, phagocytosis of debris and maintaining brain homeostasis. Brain damage results in a fast and dynamic microglia reaction, which can influence the extent and distribution of subsequent neuronal dysfunction. As a consequence, microglia responses can promote tissue protection and repair following brain injury, or become detrimental for the tissue integrity and functionality. In this review, we will describe microglia responses in the human developing brain in association with injury, with particular focus on the preterm infant. We also explore microglia responses and mechanisms of microglia toxicity in animal models of preterm white matter injury and in vitro primary microglia cell culture experiments.

AB - Microglia are the resident phagocytic cells of the central nervous system. During brain development they are also imperative for apoptosis of excessive neurons, synaptic pruning, phagocytosis of debris and maintaining brain homeostasis. Brain damage results in a fast and dynamic microglia reaction, which can influence the extent and distribution of subsequent neuronal dysfunction. As a consequence, microglia responses can promote tissue protection and repair following brain injury, or become detrimental for the tissue integrity and functionality. In this review, we will describe microglia responses in the human developing brain in association with injury, with particular focus on the preterm infant. We also explore microglia responses and mechanisms of microglia toxicity in animal models of preterm white matter injury and in vitro primary microglia cell culture experiments.

KW - Perinatal brain injury

KW - Neuroinflammation

KW - WHITE-MATTER INJURY

KW - TUMOR-NECROSIS-FACTOR

KW - BACTERIAL-ENDOTOXIN SENSITIZES

KW - ORGANOTYPIC SLICE CULTURES

KW - NITRIC-OXIDE SYNTHASE

KW - CELLS IN-VITRO

KW - ACTIVATED MICROGLIA

KW - PERIVENTRICULAR LEUKOMALACIA

KW - FETAL SHEEP

KW - GLUTAMATE-RECEPTOR

U2 - 10.1016/j.reprotox.2014.04.002

DO - 10.1016/j.reprotox.2014.04.002

M3 - Article

VL - 48

SP - 106

EP - 112

JO - Reproductive Toxicology

JF - Reproductive Toxicology

SN - 0890-6238

ER -

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