Production, regulation and role of nitric oxide in glial cells

V. A.M. Vincent; F. J.H. Tilders; A. M. Van Dam

doi:https://doi.org/10.1080/09629359890929

Production, regulation and role of nitric oxide in glial cells

V. A.M. Vincent, F. J.H. Tilders, A. M. Van Dam

Research output: Contribution to journal › Review article › Academic › peer-review

42 Citations (Scopus)

Abstract

In neuropathological conditions such as Alzheimer's disease, Parkinson's disease, AIDS dementia complex and multiple selerosis, activation of microglial cells and astroglial cells is evident. Under these neuropathological conditions cellular damage in the brain is considered to arise indirectly from cytotoxic substances produced by activated glial cells. One of these toxins is NO which has been demonstrated to be produced during several neuropathological conditions. High NO levels are produced by glial cells and exert neurotoxic effects. Astroglial cells and microglial cells communicate in various ways to reduce NO production by microglial cells which is essential to maintain homeostasis in the brain. The production of TGFβ by glial cells and its activation by astrocyte-derived tPA represents one mechanism by which astroglia limit NO production in the brain.

Original language	English
Pages (from-to)	239-255
Number of pages	17
Journal	Mediators of Inflammation
Volume	7
Issue number	4
DOIs	https://doi.org/10.1080/09629359890929
Publication status	Published - 1998

Keywords

Astroglia
Microglia
Neurodegeneration
Nitric oxide synthase
Plasminogen activators
Transforming growth factor β

Access to Document

https://doi.org/10.1080/09629359890929

Cite this

@article{581d016ed267420ca10d608e04995357,

title = "Production, regulation and role of nitric oxide in glial cells",

abstract = "In neuropathological conditions such as Alzheimer's disease, Parkinson's disease, AIDS dementia complex and multiple selerosis, activation of microglial cells and astroglial cells is evident. Under these neuropathological conditions cellular damage in the brain is considered to arise indirectly from cytotoxic substances produced by activated glial cells. One of these toxins is NO which has been demonstrated to be produced during several neuropathological conditions. High NO levels are produced by glial cells and exert neurotoxic effects. Astroglial cells and microglial cells communicate in various ways to reduce NO production by microglial cells which is essential to maintain homeostasis in the brain. The production of TGFβ by glial cells and its activation by astrocyte-derived tPA represents one mechanism by which astroglia limit NO production in the brain.",

keywords = "Astroglia, Microglia, Neurodegeneration, Nitric oxide synthase, Plasminogen activators, Transforming growth factor β",

author = "Vincent, {V. A.M.} and Tilders, {F. J.H.} and {Van Dam}, {A. M.}",

year = "1998",

doi = "https://doi.org/10.1080/09629359890929",

language = "English",

volume = "7",

pages = "239--255",

journal = "Mediators of Inflammation",

issn = "0962-9351",

publisher = "Hindawi Publishing Corporation",

number = "4",

}

TY - JOUR

T1 - Production, regulation and role of nitric oxide in glial cells

AU - Vincent, V. A.M.

AU - Tilders, F. J.H.

AU - Van Dam, A. M.

PY - 1998

Y1 - 1998

N2 - In neuropathological conditions such as Alzheimer's disease, Parkinson's disease, AIDS dementia complex and multiple selerosis, activation of microglial cells and astroglial cells is evident. Under these neuropathological conditions cellular damage in the brain is considered to arise indirectly from cytotoxic substances produced by activated glial cells. One of these toxins is NO which has been demonstrated to be produced during several neuropathological conditions. High NO levels are produced by glial cells and exert neurotoxic effects. Astroglial cells and microglial cells communicate in various ways to reduce NO production by microglial cells which is essential to maintain homeostasis in the brain. The production of TGFβ by glial cells and its activation by astrocyte-derived tPA represents one mechanism by which astroglia limit NO production in the brain.

AB - In neuropathological conditions such as Alzheimer's disease, Parkinson's disease, AIDS dementia complex and multiple selerosis, activation of microglial cells and astroglial cells is evident. Under these neuropathological conditions cellular damage in the brain is considered to arise indirectly from cytotoxic substances produced by activated glial cells. One of these toxins is NO which has been demonstrated to be produced during several neuropathological conditions. High NO levels are produced by glial cells and exert neurotoxic effects. Astroglial cells and microglial cells communicate in various ways to reduce NO production by microglial cells which is essential to maintain homeostasis in the brain. The production of TGFβ by glial cells and its activation by astrocyte-derived tPA represents one mechanism by which astroglia limit NO production in the brain.

KW - Astroglia

KW - Microglia

KW - Neurodegeneration

KW - Nitric oxide synthase

KW - Plasminogen activators

KW - Transforming growth factor β

UR - http://www.scopus.com/inward/record.url?scp=0031656992&partnerID=8YFLogxK

U2 - https://doi.org/10.1080/09629359890929

DO - https://doi.org/10.1080/09629359890929

M3 - Review article

C2 - 9792334

SN - 0962-9351

VL - 7

SP - 239

EP - 255

JO - Mediators of Inflammation

JF - Mediators of Inflammation

IS - 4

ER -

Production, regulation and role of nitric oxide in glial cells

Abstract

Keywords

Access to Document

Other files and links

Cite this