Interferon-beta protects astrocytes against tumour necrosis factor-induced apoptosis via activation of p38 mitogen-activated protein kinase.

Abstract

Several large clinical trials have demonstrated that interferon-beta (IFN-beta) therapy is effective in the treatment of multiple sclerosis (MS) patients. However, the mechanisms underlying the beneficial effects of IFN-beta are not fully understood. Most of the effort in the study of the relevant mechanisms of IFN-beta has dealt with its immunomodulatory actions. However, the beneficial effects of IFN-beta in MS patients may also depend on non-immune mechanisms, including the modulation of astrocyte function. In the present work, we have found that IFN-beta treatment protects astrocytes against tumour necrosis factor-induced apoptosis via activation of p38 mitogen-activated protein kinase. We propose that this effect may be of importance to protect astrocytes against apoptosis within the demyelinated plaques of the MS.

• Authors: Olga Barca, José A Costoya, Rosa M Señarís, Víctor M Arce
• Journal: Experimental cell research (Exp Cell Res) Vol. 314 Issue 11-12 Pg. 2231-7 (Jul 01 2008) ISSN: 1090-2422 [Electronic] United States
• PMID: 18501892 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Tumor Necrosis Factor-alpha
• Interferon-beta
• p38 Mitogen-Activated Protein Kinases

Topics

• Animals
• Apoptosis (physiology)
• Astrocytes (cytology, metabolism)
• Cells, Cultured
• Enzyme Activation
• Humans
• Interferon-beta (metabolism)
• Multiple Sclerosis (metabolism)
• Rats
• Rats, Sprague-Dawley
• Tumor Necrosis Factor-alpha (metabolism)
• p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors, genetics, metabolism)