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Interferon-beta-1beta protects against multiple sclerosis-induced endothelial cells apoptosis
Shaghayegh Haghjooy Javanmard1, Mohammad Saadatnia M, Vida Homayouni V
1Applied Physiology Research Center, Department of Physiology, Isfahan University of Medical Sciences, Hezar Jerib Avenue, Isfahan, Iran.
Frontiers in Bioscience (Elite Edition)
|December 29, 2011
Summary
Endothelial cell apoptosis damages the blood-brain barrier in multiple sclerosis (MS). Interferon beta-1b therapy reduced this apoptosis, offering a new treatment strategy for MS by protecting endothelial cells.
Area of Science:
- Neuroimmunology
- Vascular Biology
- Cellular Biology
Background:
- The blood-brain barrier (BBB) disruption from endothelial cell (EC) injury is critical in multiple sclerosis (MS) lesion development.
- Understanding EC apoptosis in MS pathophysiology is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of EC apoptosis in MS.
- To evaluate the therapeutic effect of Interferon beta-1b (IFN-beta-1b) on MS sera-induced EC apoptosis.
Main Methods:
- Human umbilical vein endothelial cells were treated with sera from MS patients (active or remission) and healthy controls.
- Apoptosis was measured using annexin V-propidium iodide staining.
- The impact of IFN-beta-1b on EC apoptosis and nitric oxide (NO) production was assessed.
Main Results:
- Sera from active MS patients significantly increased EC apoptosis compared to controls (p < 0.001).
- IFN-beta-1b at 10 U/ml blocked this apoptosis (p < 0.05) and increased NO production.
- Higher doses of IFN-beta-1b were less effective.
Conclusions:
- EC apoptosis contributes to BBB disruption in MS etiology.
- IFN-beta-1b demonstrates a novel therapeutic mechanism by inhibiting EC apoptosis in MS.
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