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Interferon-Beta-1Beta Protects Against Multiple Sclerosis-Induced Endothelial Cells Apoptosis Publisher Pubmed



Javanmard SH1 ; Mohammad Saadatnia M2, 3 ; Vida Homayouni V1 ; Mahin Nikoogoftar M4 ; Maghzi AH3, 5 ; Etemadifar M3 ; Chaitanya VG6 ; Mcgee JC7 ; Minagar A7 ; Alexander JS6
Authors
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Authors Affiliations
  1. 1. Applied Physiology Research Center, Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Hezar Jerib Avenue, Iran
  2. 2. Isfahan Medical Education Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Department of Hematology, School of Medicine, Tarbiat Modarres University, Tehran, Iran
  5. 5. Neuroimmunology Unit, Centre for Neuroscience and Trauma, Blizard Institute of Cell and Molecular Science, London, United Kingdom
  6. 6. Departments of Molecular and Cellular Physiology, Shreveport, LA 71130, 1501 Kings Highway, United States
  7. 7. Departments of Neurology, Shreveport, United States

Source: Frontiers in Bioscience - Elite Published:2012


Abstract

Disruption of the blood-brain-barrier (BBB) due to endothelial cell (EC) injury is an essential step in formation of multiple sclerosis (MS) lesions. We investigated the role of endothelial cell (EC) apoptosis in the pathophysiology of MS, studying the therapeutic effect of IFN-beta-1b against MS sera-induced endothelial apoptosis. Human umbilical vein endothelial cells were treated with sera from patients with active MS (in relapse), MS in remission, or sera from healthy volunteers (each n = 5). Apoptosis was assessed by annexin V-propidium iodide staining. Effects of IFN-beta-1b on EC apoptosis were tested at increasing doses (10, 100, and1000 U/ml). Nitrite (NO2--) levels were determined in culture supernatants. EC apoptosis was increased by sera from exacerbating MS patients, but not remission, compared to healthy individuals (p<0.001). Effects were blocked by IFN-beta-1b at 10U/ml (p<0.05), but not higher doses, and was associated with increased NO/NO2- production (p<0.05). EC apoptosis leading to disruption of the BBB may play a role in MS etiology and represents a novel therapeutic mechanism of action for IFN-beta-1b in MS therapy.
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