CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death

Science ◽  
1993 ◽  
Vol 259 (5095) ◽  
pp. 689-692 ◽  
Author(s):  
JC Louis ◽  
E Magal ◽  
S Takayama ◽  
S Varon
Keyword(s):  
Central Nervous System ◽  
Tumor Necrosis ◽  
Ciliary Neurotrophic Factor ◽  
Trophic Factor ◽  
Degenerative Diseases ◽  
Therapeutic Approaches ◽  
Tumor Necrosis Factors ◽  
The Central Nervous System ◽  
Necrosis Factor ◽  
Natural Cell

A proportion of developing oligodendrocytes undergo natural cell death by apoptosis, and mature oligodendrocytes die, either by apoptosis or necrosis, in response to injurious signals such as cytotoxic cytokines and complement. Ciliary neurotrophic factor (CNTF), a trophic factor found in astrocytes in the central nervous system (CNS), promoted the survival and maturation of cultured oligodendrocytes. This trophic factor also protected oligodendrocytes from death induced by tumor necrosis factors (apoptosis) but not against complement (necrosis). These results suggest that CNTF functions in the survival of oligodendrocytes during development and may lead to therapeutic approaches for degenerative diseases of the CNS that involve oligodendrocyte destruction.

Brain-blood permeability: TNF-α promotes escape of protein tracer from CSF to blood

2000 ◽  
Vol 279 (1) ◽  
pp. R148-R151 ◽  
Author(s):  
Jodi B. Dickstein ◽  
Harvey Moldofsky ◽  
John B. Hay
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Tumor Necrosis ◽  
Venous Blood ◽  
Protein Clearance ◽  
Tracer Recovery ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Necrosis Factor

The objective of this study was to determine the effect of tumor necrosis factor (TNF)-α on the efflux of protein from the central nervous system to blood based on assessing the clearance of radiolabeled albumin from the cerebrospinal fluid (CSF) to blood in rats. 125I-labeled human serum albumin (125I-HSA) was injected into a lateral ventricle, and venous blood was sampled hourly to determine the basal CSF protein clearance into the blood. After this, rats were intraventricularly infused with 10 μl TNF-α and 10 μl131I-HSA ( n = 6) or 10 μl saline and 10 μl 131I-HSA ( n = 6). Venous blood was sampled hourly for 3 h. 131I-HSA tracer recovery increased threefold in the venous blood and was significantly higher in the spleen, muscles, and skin in animals treated with TNF-α. No significant changes were observed in control animals treated with saline. The data suggest that TNF-α promotes the clearance of protein macromolecules from the CSF to the venous blood.

scholarly journals Tumor necrosis factor alpha induces adhesion molecule expression on human fetal astrocytes.

1992 ◽  
Vol 176 (6) ◽  
pp. 1631-1636 ◽  
Author(s):  
A A Hurwitz ◽  
W D Lyman ◽  
M P Guida ◽  
T M Calderon ◽  
J W Berman
Keyword(s):  
Central Nervous System ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Tumor Necrosis ◽  
Leukocyte Adhesion ◽  
Necrosis Factor Alpha ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Leukocyte Adhesion Molecules

Leukocyte adhesion molecules on endothelial cells of the blood-brain barrier may participate in the entry of leukocytes into the central nervous system. Because astrocytes are also a component of the blood-brain barrier and have been associated with inflammation, we studied the ability of astrocytes to express leukocyte adhesion molecules using Northern blot and immunocytochemical techniques. Astrocytes treated with the proinflammatory cytokine tumor necrosis factor alpha (TNF) expressed messenger RNA for the adhesion molecules E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1, as well as their corresponding proteins. In addition, TNF-treated astrocytes expressed a monocyte adhesion protein identified by our laboratory, recognized by the monoclonal antibody IG9. These results indicate that under inflammatory conditions in the central nervous system, such as multiple sclerosis and acquired immune deficiency syndrome, astrocyte expression of adhesion molecules may facilitate the migration of leukocytes and contribute to the disease process.

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