CNS wound healing is severely depressed in metallothionein I- and II-deficient mice

Research output: Contribution to journalJournal articleResearchpeer-review

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CNS wound healing is severely depressed in metallothionein I- and II-deficient mice. / Penkowa, M; Carrasco, J; Giralt, M; Moos, T; Hidalgo, J.

In: Journal of Neuroscience, Vol. 19, No. 7, 1999, p. 2535-2545.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Penkowa, M, Carrasco, J, Giralt, M, Moos, T & Hidalgo, J 1999, 'CNS wound healing is severely depressed in metallothionein I- and II-deficient mice', Journal of Neuroscience, vol. 19, no. 7, pp. 2535-2545.

APA

Penkowa, M., Carrasco, J., Giralt, M., Moos, T., & Hidalgo, J. (1999). CNS wound healing is severely depressed in metallothionein I- and II-deficient mice. Journal of Neuroscience, 19(7), 2535-2545.

Vancouver

Penkowa M, Carrasco J, Giralt M, Moos T, Hidalgo J. CNS wound healing is severely depressed in metallothionein I- and II-deficient mice. Journal of Neuroscience. 1999;19(7):2535-2545.

Author

Penkowa, M ; Carrasco, J ; Giralt, M ; Moos, T ; Hidalgo, J. / CNS wound healing is severely depressed in metallothionein I- and II-deficient mice. In: Journal of Neuroscience. 1999 ; Vol. 19, No. 7. pp. 2535-2545.

Bibtex

@article{ef7e3ab074c811dbbee902004c4f4f50,
title = "CNS wound healing is severely depressed in metallothionein I- and II-deficient mice",
abstract = "To characterize the physiological role of metallothioneins I and II (MT-I+II) in the brain, we have examined the chronological effects of a freeze injury to the cortex in normal and MT-I+II null mice. In normal mice, microglia/macrophage activation and astrocytosis were observed in the areas surrounding the lesion site, peaking at approximately 1 and 3 d postlesion (dpl), respectively. At 20 dpl, the parenchyma had regenerated. Both brain macrophages and astrocytes surrounding the lesion increased the MT-I+II immunoreactivity, peaking at approximately 3 dpl, and at 20 dpl it was similar to that of unlesioned mice. In situ hybridization analysis indicates that MT-I+II immunoreactivity reflects changes in the messenger levels. In MT-I+II null mice, microglia/macrophages infiltrated the lesion heavily, and at 20 dpl they were still present. Reactive astrocytosis was delayed and persisted at 20 dpl. In contrast to normal mice, at 20 dpl no wound healing had occurred. The rate of apoptosis, as determined by using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, was drastically increased in neurons of ipsilateral cortex of the MT-I+II null mice. Our results demonstrate that MT-I+II are essential for a normal wound repair in the CNS, and that their deficiency impairs neuronal survival.",
keywords = "Faculty of Health and Medical Sciences, Astrocytes, In Situ Hybridization, In Situ Nick-End Labeling, Macrophages, Knockout, Mice, Microglia, Neurons, Staining and Labeling, Superoxide Dismutase, Wound Healing",
author = "M Penkowa and J Carrasco and M Giralt and T Moos and J Hidalgo",
year = "1999",
language = "English",
volume = "19",
pages = "2535--2545",
journal = "The Journal of neuroscience : the official journal of the Society for Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "7",

}

RIS

TY - JOUR

T1 - CNS wound healing is severely depressed in metallothionein I- and II-deficient mice

AU - Penkowa, M

AU - Carrasco, J

AU - Giralt, M

AU - Moos, T

AU - Hidalgo, J

PY - 1999

Y1 - 1999

N2 - To characterize the physiological role of metallothioneins I and II (MT-I+II) in the brain, we have examined the chronological effects of a freeze injury to the cortex in normal and MT-I+II null mice. In normal mice, microglia/macrophage activation and astrocytosis were observed in the areas surrounding the lesion site, peaking at approximately 1 and 3 d postlesion (dpl), respectively. At 20 dpl, the parenchyma had regenerated. Both brain macrophages and astrocytes surrounding the lesion increased the MT-I+II immunoreactivity, peaking at approximately 3 dpl, and at 20 dpl it was similar to that of unlesioned mice. In situ hybridization analysis indicates that MT-I+II immunoreactivity reflects changes in the messenger levels. In MT-I+II null mice, microglia/macrophages infiltrated the lesion heavily, and at 20 dpl they were still present. Reactive astrocytosis was delayed and persisted at 20 dpl. In contrast to normal mice, at 20 dpl no wound healing had occurred. The rate of apoptosis, as determined by using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, was drastically increased in neurons of ipsilateral cortex of the MT-I+II null mice. Our results demonstrate that MT-I+II are essential for a normal wound repair in the CNS, and that their deficiency impairs neuronal survival.

AB - To characterize the physiological role of metallothioneins I and II (MT-I+II) in the brain, we have examined the chronological effects of a freeze injury to the cortex in normal and MT-I+II null mice. In normal mice, microglia/macrophage activation and astrocytosis were observed in the areas surrounding the lesion site, peaking at approximately 1 and 3 d postlesion (dpl), respectively. At 20 dpl, the parenchyma had regenerated. Both brain macrophages and astrocytes surrounding the lesion increased the MT-I+II immunoreactivity, peaking at approximately 3 dpl, and at 20 dpl it was similar to that of unlesioned mice. In situ hybridization analysis indicates that MT-I+II immunoreactivity reflects changes in the messenger levels. In MT-I+II null mice, microglia/macrophages infiltrated the lesion heavily, and at 20 dpl they were still present. Reactive astrocytosis was delayed and persisted at 20 dpl. In contrast to normal mice, at 20 dpl no wound healing had occurred. The rate of apoptosis, as determined by using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, was drastically increased in neurons of ipsilateral cortex of the MT-I+II null mice. Our results demonstrate that MT-I+II are essential for a normal wound repair in the CNS, and that their deficiency impairs neuronal survival.

KW - Faculty of Health and Medical Sciences

KW - Astrocytes

KW - In Situ Hybridization

KW - In Situ Nick-End Labeling

KW - Macrophages

KW - Knockout

KW - Mice

KW - Microglia

KW - Neurons

KW - Staining and Labeling

KW - Superoxide Dismutase

KW - Wound Healing

M3 - Journal article

C2 - 10087067

VL - 19

SP - 2535

EP - 2545

JO - The Journal of neuroscience : the official journal of the Society for Neuroscience

JF - The Journal of neuroscience : the official journal of the Society for Neuroscience

SN - 0270-6474

IS - 7

ER -

ID: 190519