Astrocytic β2-adrenergic receptors and multiple sclerosis

Despite intensive research, the cause and a cure of multiple sclerosis (MS) have remained elusive and many aspects of the pathogenesis are not understood. Immunohistochemical experiments have shown that astrocytic β2-adrenergic receptors are lost in MS. Because norepinephrine mediates important supp...

Ամբողջական նկարագրություն

Մատենագիտական մանրամասներ
Հիմնական հեղինակներ: Jacques De Keyser, Esther Zeinstra, Nadine Wilczak
Ձևաչափ: Հոդված
Լեզու:English
Հրապարակվել է: Elsevier 2004-03-01
Շարք:Neurobiology of Disease
Խորագրեր:
Առցանց հասանելիություն:http://www.sciencedirect.com/science/article/pii/S0969996103002481
_version_ 1828968324099211264
author Jacques De Keyser
Esther Zeinstra
Nadine Wilczak
author_facet Jacques De Keyser
Esther Zeinstra
Nadine Wilczak
author_sort Jacques De Keyser
collection DOAJ
description Despite intensive research, the cause and a cure of multiple sclerosis (MS) have remained elusive and many aspects of the pathogenesis are not understood. Immunohistochemical experiments have shown that astrocytic β2-adrenergic receptors are lost in MS. Because norepinephrine mediates important supportive and protective actions of astrocytes via activation of these β2-adrenergic receptors, we postulate that this abnormality may play a prominent role in the pathogenesis of MS. First, it may allow astrocytes to act as facultative antigen-presenting cells, thereby initiating T-cell mediated inflammatory responses that lead to the characteristic demyelinated lesions. Second, it may contribute to inflammatory injury by stimulating the production of nitric oxide and proinflammatory cytokines, and reducing glutamate uptake. Third, it may lead to apoptosis of oligodendrocytes by reducing the astrocytic production of trophic factors, including neuregulin, nerve growth factor and brain-derived neurotrophic factor. Fourth, it may impair astrocytic glycogenolysis, which supplies energy to axons, and this may represent a mechanism underlying axonal degeneration that is hold responsible for the progressive chronic disability.
first_indexed 2024-12-14T12:09:30Z
format Article
id doaj.art-baf566b9d2bc41159c51a2f30c1b9ab8
institution Directory Open Access Journal
issn 1095-953X
language English
last_indexed 2024-12-14T12:09:30Z
publishDate 2004-03-01
publisher Elsevier
record_format Article
series Neurobiology of Disease
spelling doaj.art-baf566b9d2bc41159c51a2f30c1b9ab82022-12-21T23:01:48ZengElsevierNeurobiology of Disease1095-953X2004-03-01152331339Astrocytic β2-adrenergic receptors and multiple sclerosisJacques De Keyser0Esther Zeinstra1Nadine Wilczak2Department of Neurology, University Hospital Groningen, Groningen, The NetherlandsDepartment of Neurology, University Hospital Groningen, Groningen, The NetherlandsDepartment of Neurology, University Hospital Groningen, Groningen, The NetherlandsDespite intensive research, the cause and a cure of multiple sclerosis (MS) have remained elusive and many aspects of the pathogenesis are not understood. Immunohistochemical experiments have shown that astrocytic β2-adrenergic receptors are lost in MS. Because norepinephrine mediates important supportive and protective actions of astrocytes via activation of these β2-adrenergic receptors, we postulate that this abnormality may play a prominent role in the pathogenesis of MS. First, it may allow astrocytes to act as facultative antigen-presenting cells, thereby initiating T-cell mediated inflammatory responses that lead to the characteristic demyelinated lesions. Second, it may contribute to inflammatory injury by stimulating the production of nitric oxide and proinflammatory cytokines, and reducing glutamate uptake. Third, it may lead to apoptosis of oligodendrocytes by reducing the astrocytic production of trophic factors, including neuregulin, nerve growth factor and brain-derived neurotrophic factor. Fourth, it may impair astrocytic glycogenolysis, which supplies energy to axons, and this may represent a mechanism underlying axonal degeneration that is hold responsible for the progressive chronic disability.http://www.sciencedirect.com/science/article/pii/S0969996103002481Multiple sclerosisBeta2 adrenergic receptorsAstrocytesPathophysiology
spellingShingle Jacques De Keyser
Esther Zeinstra
Nadine Wilczak
Astrocytic β2-adrenergic receptors and multiple sclerosis
Neurobiology of Disease
Multiple sclerosis
Beta2 adrenergic receptors
Astrocytes
Pathophysiology
title Astrocytic β2-adrenergic receptors and multiple sclerosis
title_full Astrocytic β2-adrenergic receptors and multiple sclerosis
title_fullStr Astrocytic β2-adrenergic receptors and multiple sclerosis
title_full_unstemmed Astrocytic β2-adrenergic receptors and multiple sclerosis
title_short Astrocytic β2-adrenergic receptors and multiple sclerosis
title_sort astrocytic β2 adrenergic receptors and multiple sclerosis
topic Multiple sclerosis
Beta2 adrenergic receptors
Astrocytes
Pathophysiology
url http://www.sciencedirect.com/science/article/pii/S0969996103002481
work_keys_str_mv AT jacquesdekeyser astrocyticb2adrenergicreceptorsandmultiplesclerosis
AT estherzeinstra astrocyticb2adrenergicreceptorsandmultiplesclerosis
AT nadinewilczak astrocyticb2adrenergicreceptorsandmultiplesclerosis