NDLI: HMGB1 in Development and Diseases of the Central Nervous System

Content Provider	Springer Nature Link
Author	Fang, Ping Schachner, Melitta Shen, Yan Qin
Copyright Year	2012
Abstract	High mobility group box 1 (HMGB1) is widely expressed in cells of vertebrates in two forms: a nuclear “architectural” factor and a secreted inflammatory factor. During early brain development, HMGB1 displays a complex temporal and spatial distribution pattern in the central nervous system. It facilitates neurite outgrowth and cell migration critical for processes, such as forebrain development. During adulthood, HMGB1 serves to induce neuroinflammation after injury, such as lesions in the spinal cord and brain. Receptor for advanced glycation end products and Toll-like receptors signal transduction pathways mediate HMGB1-induced neuroinflammation and necrosis. Increased levels of endogenous HMGB1 have also been detected in neurodegenerative diseases. However, in Huntington’s disease, HMGB1 has been reported to protect neurons through activation of apurinic/apyrimidinic endonuclease and 5′-flap endonuclease-1, whereas in other neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, HMGB1 serves as a risk factor for memory impairment, chronic neurodegeneration, and progression of neuroinflammation. Thus, HMGB1 plays important and double-edged roles during neural development and neurodegeneration. The HMGB1-mediated pathological mechanisms have remained largely elusive. Knowledge of these mechanisms is likely to lead to therapeutic targets for neurological diseases.
Starting Page	499
Ending Page	506
Page Count	8
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	45
Issue Number	3
e-ISSN	15591182
Language	English
Publisher	Humana Press Inc
Publisher Date	2012-05-13
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	HMGB1 Nervous system Neural development Neuroinflammation Neurodegeneration Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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