Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury

Julien Pansiot; Hoa Pham; Jeremie Dalous; Didier Chevenne; Marina Colella; Leslie Schwendimann; Assia Fafouri; Jérôme Mairesse; Raffaella Moretti; Anne-Laure Schang; Christiane Charriaut-Marlangue; Pierre Gressens; Olivier Baud

doi:10.1016/j.expneurol.2016.05.024

Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury

Julien Pansiot, Hoa Pham, Jeremie Dalous, Didier Chevenne, Marina Colella, Leslie Schwendimann, Assia Fafouri, Jérôme Mairesse, Raffaella Moretti, Anne-Laure Schang, Christiane Charriaut-Marlangue, Pierre Gressens, Olivier Baud

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Abstract

White-matter injury is the most common cause of the adverse neurodevelopmental outcomes observed in preterm infants. Only few options exist to prevent perinatal brain injury associated to preterm delivery. 17β-estradiol (E2) is the predominant estrogen in circulation and has been shown to be neuroprotective in vitro and in vivo. However, while E2 has been found to modulate inflammation in adult models of brain damage, how estrogens influence glial cells response in the developing brain needs further investigations. Using a model of ibotenate-induced brain injury, we have refined the effects of E2 in the developing brain. E2 provides significant neuroprotection both in the cortical plate and the white matter in neonatal rats subjected to excitotoxic insult mimicking white matter and cortical damages frequently observed in very preterm infants. E2 promotes significant changes in microglial phenotypes balance in response to brain injury and the acceleration of oligodendrocyte maturation. Maturational effects of E2 on myelination process were observed both in vivo and in vitro. Altogether, these data demonstrate that response of glial cells to E2 could be responsible for its neuroprotective properties in neonatal excitotoxic brain injury.

Original language	English
Pages (from-to)	56-65
Number of pages	10
Journal	Experimental Neurology
Volume	282
Early online date	21 May 2016
DOIs	https://doi.org/10.1016/j.expneurol.2016.05.024
Publication status	Published - Aug 2016

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10.1016/j.expneurol.2016.05.024

Glial response to 17β-estradiol_PANSIOT_Accepted19May2016_GREEN AAMAccepted author manuscript, 601 KBLicence: CC BY-NC-ND

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title = "Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury",

abstract = "White-matter injury is the most common cause of the adverse neurodevelopmental outcomes observed in preterm infants. Only few options exist to prevent perinatal brain injury associated to preterm delivery. 17β-estradiol (E2) is the predominant estrogen in circulation and has been shown to be neuroprotective in vitro and in vivo. However, while E2 has been found to modulate inflammation in adult models of brain damage, how estrogens influence glial cells response in the developing brain needs further investigations. Using a model of ibotenate-induced brain injury, we have refined the effects of E2 in the developing brain. E2 provides significant neuroprotection both in the cortical plate and the white matter in neonatal rats subjected to excitotoxic insult mimicking white matter and cortical damages frequently observed in very preterm infants. E2 promotes significant changes in microglial phenotypes balance in response to brain injury and the acceleration of oligodendrocyte maturation. Maturational effects of E2 on myelination process were observed both in vivo and in vitro. Altogether, these data demonstrate that response of glial cells to E2 could be responsible for its neuroprotective properties in neonatal excitotoxic brain injury.",

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year = "2016",

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doi = "10.1016/j.expneurol.2016.05.024",

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T1 - Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury

AU - Pansiot, Julien

AU - Pham, Hoa

AU - Dalous, Jeremie

AU - Chevenne, Didier

AU - Colella, Marina

AU - Schwendimann, Leslie

AU - Fafouri, Assia

AU - Mairesse, Jérôme

AU - Moretti, Raffaella

AU - Schang, Anne-Laure

AU - Charriaut-Marlangue, Christiane

AU - Gressens, Pierre

AU - Baud, Olivier

PY - 2016/8

Y1 - 2016/8

N2 - White-matter injury is the most common cause of the adverse neurodevelopmental outcomes observed in preterm infants. Only few options exist to prevent perinatal brain injury associated to preterm delivery. 17β-estradiol (E2) is the predominant estrogen in circulation and has been shown to be neuroprotective in vitro and in vivo. However, while E2 has been found to modulate inflammation in adult models of brain damage, how estrogens influence glial cells response in the developing brain needs further investigations. Using a model of ibotenate-induced brain injury, we have refined the effects of E2 in the developing brain. E2 provides significant neuroprotection both in the cortical plate and the white matter in neonatal rats subjected to excitotoxic insult mimicking white matter and cortical damages frequently observed in very preterm infants. E2 promotes significant changes in microglial phenotypes balance in response to brain injury and the acceleration of oligodendrocyte maturation. Maturational effects of E2 on myelination process were observed both in vivo and in vitro. Altogether, these data demonstrate that response of glial cells to E2 could be responsible for its neuroprotective properties in neonatal excitotoxic brain injury.

AB - White-matter injury is the most common cause of the adverse neurodevelopmental outcomes observed in preterm infants. Only few options exist to prevent perinatal brain injury associated to preterm delivery. 17β-estradiol (E2) is the predominant estrogen in circulation and has been shown to be neuroprotective in vitro and in vivo. However, while E2 has been found to modulate inflammation in adult models of brain damage, how estrogens influence glial cells response in the developing brain needs further investigations. Using a model of ibotenate-induced brain injury, we have refined the effects of E2 in the developing brain. E2 provides significant neuroprotection both in the cortical plate and the white matter in neonatal rats subjected to excitotoxic insult mimicking white matter and cortical damages frequently observed in very preterm infants. E2 promotes significant changes in microglial phenotypes balance in response to brain injury and the acceleration of oligodendrocyte maturation. Maturational effects of E2 on myelination process were observed both in vivo and in vitro. Altogether, these data demonstrate that response of glial cells to E2 could be responsible for its neuroprotective properties in neonatal excitotoxic brain injury.

U2 - 10.1016/j.expneurol.2016.05.024

DO - 10.1016/j.expneurol.2016.05.024

M3 - Article

C2 - 27222132

SN - 0014-4886

VL - 282

SP - 56

EP - 65

JO - Experimental Neurology

JF - Experimental Neurology

ER -

Glial response to 17β-estradiol in neonatal rats with excitotoxic brain injury

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