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Metallothionein‐I+II in neuroprotection
Author(s) -
Pedersen Mie Ø.,
Jensen Rikke,
Pedersen Dan S.,
Skjolding Anders D.,
Hempel Casper,
Maretty Lasse,
Penkowa Milena
Publication year - 2009
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.44
Subject(s) - neuroprotection , microbiology and biotechnology , neurodegeneration , lrp1 , oxidative stress , chemistry , reactive oxygen species , inflammation , glial scar , central nervous system , biology , neuroscience , immunology , biochemistry , astrocyte , lipoprotein , medicine , ldl receptor , pathology , disease , cholesterol
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. © 2009 International Union of Biochemistry and Molecular Biology, Inc.