Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury

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Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury. / Penkowa, Milena; Giralt, Mercedes; Lago, Natalia; Camats, Jordi; Carrasco, Javier; Hernández, Joaquin; Molinero, Amalia; Campbell, Iain L; Hidalgo, Juan.

I: Experimental Neurology, Bind 181, Nr. 2, 2003, s. 130-148.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Penkowa, M, Giralt, M, Lago, N, Camats, J, Carrasco, J, Hernández, J, Molinero, A, Campbell, IL & Hidalgo, J 2003, 'Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury', Experimental Neurology, bind 181, nr. 2, s. 130-148. https://doi.org/10.1016/S0014-4886(02)00051-1

APA

Penkowa, M., Giralt, M., Lago, N., Camats, J., Carrasco, J., Hernández, J., Molinero, A., Campbell, I. L., & Hidalgo, J. (2003). Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury. Experimental Neurology, 181(2), 130-148. https://doi.org/10.1016/S0014-4886(02)00051-1

Vancouver

Penkowa M, Giralt M, Lago N, Camats J, Carrasco J, Hernández J o.a. Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury. Experimental Neurology. 2003;181(2):130-148. https://doi.org/10.1016/S0014-4886(02)00051-1

Author

Penkowa, Milena ; Giralt, Mercedes ; Lago, Natalia ; Camats, Jordi ; Carrasco, Javier ; Hernández, Joaquin ; Molinero, Amalia ; Campbell, Iain L ; Hidalgo, Juan. / Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury. I: Experimental Neurology. 2003 ; Bind 181, Nr. 2. s. 130-148.

Bibtex

@article{e6cf781074c411dbbee902004c4f4f50,
title = "Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury",
abstract = "The effect of CNS-targeted IL-6 gene expression has been thoroughly investigated in the otherwise nonperturbed brain but not following brain injury. Here we examined the impact of astrocyte-targeted IL-6 production in a traumatic brain injury (cryolesion) model using GFAP-IL6 transgenic mice. This study demonstrated that transgenic IL-6 production significantly increased wound healing following the cryolesion. Thus, at 20 days postlesion (dpl) the GFAP-IL6 mice showed almost complete wound healing compared to litter mate nontransgenic controls. It seems likely that a reduced inflammatory response in the long term could be responsible for this IL-6-related effect. Thus, while in the acute phase following cryolesion (1-6 dpl) the recruitment of macrophages and T lymphocytes was higher in GFAP-IL6 mice, at 10-20 dpl it was significantly reduced compared to controls. Reactive astrogliosis was also significantly increased up to but not including 20 dpl in the GFAP-IL6 mice. Oxidative stress as well as apoptotic cell death was significantly decreased throughout the time period studied in the GFAP-IL6 mice compared to controls. This could be linked to the altered inflammatory response as well as to the transgenic IL-6-induced increase of the antioxidant, neuroprotective proteins metallothionein-I + II. These results indicate that although in the brain the chronic astrocyte-targeted expression of IL-6 spontaneously induces an inflammatory response causing significant damage, during an acute neuropathological insult such as following traumatic injury, a clear neuroprotective role is evident.",
keywords = "Faculty of Health and Medical Sciences, Animals, Antioxidants, Apoptosis, Astrocytes, Brain Injuries, Central Nervous System, Cerebral Cortex, Disease Models, Gene Targeting, Gliosis, Interleukin-6, Lymphocytes, Macrophages, Transgenic, Oxidative Stress, Wound Healing",
author = "Milena Penkowa and Mercedes Giralt and Natalia Lago and Jordi Camats and Javier Carrasco and Joaquin Hern{\'a}ndez and Amalia Molinero and Campbell, {Iain L} and Juan Hidalgo",
year = "2003",
doi = "10.1016/S0014-4886(02)00051-1",
language = "English",
volume = "181",
pages = "130--148",
journal = "Experimental Neurology",
issn = "0014-4886",
publisher = "Academic Press",
number = "2",

}

RIS

TY - JOUR

T1 - Astrocyte-targeted expression of IL-6 protects the CNS against a focal brain injury

AU - Penkowa, Milena

AU - Giralt, Mercedes

AU - Lago, Natalia

AU - Camats, Jordi

AU - Carrasco, Javier

AU - Hernández, Joaquin

AU - Molinero, Amalia

AU - Campbell, Iain L

AU - Hidalgo, Juan

PY - 2003

Y1 - 2003

N2 - The effect of CNS-targeted IL-6 gene expression has been thoroughly investigated in the otherwise nonperturbed brain but not following brain injury. Here we examined the impact of astrocyte-targeted IL-6 production in a traumatic brain injury (cryolesion) model using GFAP-IL6 transgenic mice. This study demonstrated that transgenic IL-6 production significantly increased wound healing following the cryolesion. Thus, at 20 days postlesion (dpl) the GFAP-IL6 mice showed almost complete wound healing compared to litter mate nontransgenic controls. It seems likely that a reduced inflammatory response in the long term could be responsible for this IL-6-related effect. Thus, while in the acute phase following cryolesion (1-6 dpl) the recruitment of macrophages and T lymphocytes was higher in GFAP-IL6 mice, at 10-20 dpl it was significantly reduced compared to controls. Reactive astrogliosis was also significantly increased up to but not including 20 dpl in the GFAP-IL6 mice. Oxidative stress as well as apoptotic cell death was significantly decreased throughout the time period studied in the GFAP-IL6 mice compared to controls. This could be linked to the altered inflammatory response as well as to the transgenic IL-6-induced increase of the antioxidant, neuroprotective proteins metallothionein-I + II. These results indicate that although in the brain the chronic astrocyte-targeted expression of IL-6 spontaneously induces an inflammatory response causing significant damage, during an acute neuropathological insult such as following traumatic injury, a clear neuroprotective role is evident.

AB - The effect of CNS-targeted IL-6 gene expression has been thoroughly investigated in the otherwise nonperturbed brain but not following brain injury. Here we examined the impact of astrocyte-targeted IL-6 production in a traumatic brain injury (cryolesion) model using GFAP-IL6 transgenic mice. This study demonstrated that transgenic IL-6 production significantly increased wound healing following the cryolesion. Thus, at 20 days postlesion (dpl) the GFAP-IL6 mice showed almost complete wound healing compared to litter mate nontransgenic controls. It seems likely that a reduced inflammatory response in the long term could be responsible for this IL-6-related effect. Thus, while in the acute phase following cryolesion (1-6 dpl) the recruitment of macrophages and T lymphocytes was higher in GFAP-IL6 mice, at 10-20 dpl it was significantly reduced compared to controls. Reactive astrogliosis was also significantly increased up to but not including 20 dpl in the GFAP-IL6 mice. Oxidative stress as well as apoptotic cell death was significantly decreased throughout the time period studied in the GFAP-IL6 mice compared to controls. This could be linked to the altered inflammatory response as well as to the transgenic IL-6-induced increase of the antioxidant, neuroprotective proteins metallothionein-I + II. These results indicate that although in the brain the chronic astrocyte-targeted expression of IL-6 spontaneously induces an inflammatory response causing significant damage, during an acute neuropathological insult such as following traumatic injury, a clear neuroprotective role is evident.

KW - Faculty of Health and Medical Sciences

KW - Animals

KW - Antioxidants

KW - Apoptosis

KW - Astrocytes

KW - Brain Injuries

KW - Central Nervous System

KW - Cerebral Cortex

KW - Disease Models

KW - Gene Targeting

KW - Gliosis

KW - Interleukin-6

KW - Lymphocytes

KW - Macrophages

KW - Transgenic

KW - Oxidative Stress

KW - Wound Healing

U2 - 10.1016/S0014-4886(02)00051-1

DO - 10.1016/S0014-4886(02)00051-1

M3 - Journal article

C2 - 12781987

VL - 181

SP - 130

EP - 148

JO - Experimental Neurology

JF - Experimental Neurology

SN - 0014-4886

IS - 2

ER -

ID: 121592