IMR Press / FBE / Volume 4 / Issue 4 / DOI: 10.2741/e466

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Interferon-beta-1beta protects against multiple sclerosis-induced endothelial cells apoptosis

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1 Applied Physiology Research Center, Department of Physiology, Isfahan University of Medical Sciences, Hezar Jerib Avenue, Isfahan, Iran
2 Isfahan Medical Education Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
3 Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Hematology, School of Medicine, Tarbiat Modarres University, Tehran, Iran
5 Neuroimmunology unit, Centre for Neuroscience & Trauma, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
6 Departments of Molecular and Cellular Physiology, Shreveport, USA, Shreveport, USA
7 Departments of Neurologym, Shreveport, USA

*Author to whom correspondence should be addressed.

 

Front. Biosci. (Elite Ed) 2012, 4(4), 1368–1374; https://doi.org/10.2741/e466
Published: 1 January 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.

Keywords
Multiple sclerosis
Nitric Oxide
Endothelial Cell
Apoptosis
Interferon-Beta
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