Metallothionein-I+II in neuroprotection

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Metallothionein-I+II in neuroprotection. / Pedersen, Mie Ø; Jensen, Rikke; Pedersen, Dan S; Skjolding, Anders D; Hempel, Casper; Maretty, Lasse; Penkowa, Milena.

In: BioFactors, Vol. 35, No. 4, 2009, p. 315-325.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Pedersen, MØ, Jensen, R, Pedersen, DS, Skjolding, AD, Hempel, C, Maretty, L & Penkowa, M 2009, 'Metallothionein-I+II in neuroprotection', BioFactors, vol. 35, no. 4, pp. 315-325. https://doi.org/10.1002/biof.44

APA

Pedersen, M. Ø., Jensen, R., Pedersen, D. S., Skjolding, A. D., Hempel, C., Maretty, L., & Penkowa, M. (2009). Metallothionein-I+II in neuroprotection. BioFactors, 35(4), 315-325. https://doi.org/10.1002/biof.44

Vancouver

Pedersen MØ, Jensen R, Pedersen DS, Skjolding AD, Hempel C, Maretty L et al. Metallothionein-I+II in neuroprotection. BioFactors. 2009;35(4):315-325. https://doi.org/10.1002/biof.44

Author

Pedersen, Mie Ø ; Jensen, Rikke ; Pedersen, Dan S ; Skjolding, Anders D ; Hempel, Casper ; Maretty, Lasse ; Penkowa, Milena. / Metallothionein-I+II in neuroprotection. In: BioFactors. 2009 ; Vol. 35, No. 4. pp. 315-325.

Bibtex

@article{3dc9d9b0832911de8bc9000ea68e967b,
title = "Metallothionein-I+II in neuroprotection",
abstract = "Metallothionein (MT)-I+II synthesis is induced in the central nervous system (CNS) in response to practically any pathogen or disorder, where it is increased mainly in reactive glia. MT-I+II are involved in host defence reactions and neuroprotection during neuropathological conditions, in which MT-I+II decrease inflammation and secondary tissue damage (oxidative stress, neurodegeneration, and apoptosis) and promote post-injury repair and regeneration (angiogenesis, neurogenesis, neuronal sprouting and tissue remodelling). Intracellularly the molecular MT-I+II actions involve metal ion control and scavenging of reactive oxygen species (ROS) leading to cellular redox control. By regulating metal ions, MT-I+II can control metal-containing transcription factors, zinc-finger proteins and p53. However, the neuroprotective functions of MT-I+II also involve an extracellular component. MT-I+II protects the neurons by signal transduction through the low-density lipoprotein family of receptors on the cell surface involving lipoprotein receptor-1 (LRP1) and megalin (LRP2). In this review we discuss the newest data on cerebral MT-I+II functions following brain injury and experimental autoimmune encephalomyelitis. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.",
author = "Pedersen, {Mie {\O}} and Rikke Jensen and Pedersen, {Dan S} and Skjolding, {Anders D} and Casper Hempel and Lasse Maretty and Milena Penkowa",
year = "2009",
doi = "10.1002/biof.44",
language = "English",
volume = "35",
pages = "315--325",
journal = "BioFactors",
issn = "0951-6433",
publisher = "Wiley",
number = "4",

}

RIS

TY - JOUR

T1 - Metallothionein-I+II in neuroprotection

AU - Pedersen, Mie Ø

AU - Jensen, Rikke

AU - Pedersen, Dan S

AU - Skjolding, Anders D

AU - Hempel, Casper

AU - Maretty, Lasse

AU - Penkowa, Milena

PY - 2009

Y1 - 2009

N2 - Metallothionein (MT)-I+II synthesis is induced in the central nervous system (CNS) in response to practically any pathogen or disorder, where it is increased mainly in reactive glia. MT-I+II are involved in host defence reactions and neuroprotection during neuropathological conditions, in which MT-I+II decrease inflammation and secondary tissue damage (oxidative stress, neurodegeneration, and apoptosis) and promote post-injury repair and regeneration (angiogenesis, neurogenesis, neuronal sprouting and tissue remodelling). Intracellularly the molecular MT-I+II actions involve metal ion control and scavenging of reactive oxygen species (ROS) leading to cellular redox control. By regulating metal ions, MT-I+II can control metal-containing transcription factors, zinc-finger proteins and p53. However, the neuroprotective functions of MT-I+II also involve an extracellular component. MT-I+II protects the neurons by signal transduction through the low-density lipoprotein family of receptors on the cell surface involving lipoprotein receptor-1 (LRP1) and megalin (LRP2). In this review we discuss the newest data on cerebral MT-I+II functions following brain injury and experimental autoimmune encephalomyelitis. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.

AB - Metallothionein (MT)-I+II synthesis is induced in the central nervous system (CNS) in response to practically any pathogen or disorder, where it is increased mainly in reactive glia. MT-I+II are involved in host defence reactions and neuroprotection during neuropathological conditions, in which MT-I+II decrease inflammation and secondary tissue damage (oxidative stress, neurodegeneration, and apoptosis) and promote post-injury repair and regeneration (angiogenesis, neurogenesis, neuronal sprouting and tissue remodelling). Intracellularly the molecular MT-I+II actions involve metal ion control and scavenging of reactive oxygen species (ROS) leading to cellular redox control. By regulating metal ions, MT-I+II can control metal-containing transcription factors, zinc-finger proteins and p53. However, the neuroprotective functions of MT-I+II also involve an extracellular component. MT-I+II protects the neurons by signal transduction through the low-density lipoprotein family of receptors on the cell surface involving lipoprotein receptor-1 (LRP1) and megalin (LRP2). In this review we discuss the newest data on cerebral MT-I+II functions following brain injury and experimental autoimmune encephalomyelitis. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.

U2 - 10.1002/biof.44

DO - 10.1002/biof.44

M3 - Journal article

C2 - 19655389

VL - 35

SP - 315

EP - 325

JO - BioFactors

JF - BioFactors

SN - 0951-6433

IS - 4

ER -

ID: 13619983