aBrain Mapping Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
bBiochemistry Department, Faculty of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran
Log in to MyKarger to check if you already have access to this content.
Buy FullText & PDF Unlimited re-access via MyKarger Unrestricted printing, no saving restrictions for personal use read more
CHF 38.00 *
EUR 35.00 *
USD 39.00 *
Buy a Karger Article Bundle (KAB) and profit from a discount!
If you would like to redeem your KAB credit, please log in.
Save over 20% compared to the individual article price. Access via DeepDyve Unlimited fulltext viewing Of this article Organize, annotate And mark up articles Printing And downloading restrictions apply Subscribe Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use read more Select* The final prices may differ from the prices shown due to specifics of VAT rules.
Article / Publication DetailsFirst-Page Preview
Received: December 21, 2021
Accepted: June 07, 2022
Published online: August 18, 2022
Number of Print Pages: 10
Number of Figures: 6
Number of Tables: 5
ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)
For additional information: https://www.karger.com/NIM
AbstractBackground: Growing bodies of evidence suggest that angiogenesis plays a crucial role in the development and progression of multiple sclerosis (MS). Vascular endothelial growth factor (VEGF) is one of the key factors involved in angiogenesis. Because of this importance, we investigated the serum levels of VEGF in MS patients according to their clinical phase and subtype of MS in this study. Material and Methods: This case-control study was done on 47 definite MS patients with the first clinical attack and 47 randomly selected individuals without any underlying inflammatory and autoimmune disease as the control group. The total serum VEGF level was measured from the subject’s peripheral blood sample by ELISA during the first and second attacks of MS and 6 months after the first attack in the remission phase as well as the control group. In addition, the correlation between these variables and the influence of gender, age, and duration of the remission phase on such associations was evaluated by using the independent t test and Pearson’s correlation coefficient. Results: There was an increase in the serum level of VEGF in all phases of MS compared with non-MS individuals (p value <0.0001) and a significant correlation between the serum level of VEGF and the interval between first and second attacks (r = −720, p < 0.0001). A higher serum level of VEGF in the first attack leads to higher VEGF levels in the second and sixth mount of remission phases. Conclusion: Rise in the serum VEGF level may be involved in MS’s relapsing phases and a shorter remission phase. Therefore, it could be used as a prognostic and predictive biomarker for MS disease.
© 2022 S. Karger AG, Basel
References Loma I, Heyman R. Multiple sclerosis: pathogenesis and treatment. Curr Neuropharmacol. 2011;9(3):409–16. Lutton J, Winston R, Rodman T. Multiple sclerosis: etiological mechanisms and future directions. Exp Biol Med. 2004;229(1):12–20. Pakpoor J, Giovannoni G, Ramagopalan SV. Epstein-Barr virus and multiple sclerosis: association or causation? Expert Rev Neurother. 2013;13(3):287–97. Sawcer S, Franklin RJ, Ban M. Multiple sclerosis genetics. Lancet Neurol. 2014;13(7):700–9. Pakpoor J, Disanto G, Gerber JE, Dobson R, Meier UC, Giovannoni G, et al. The risk of developing multiple sclerosis in individuals seronegative for Epstein-Barr virus: a meta-analysis. Mult Scler. 2013;19(2):162–6. Frohman EM, Racke MK, Raine CS. Multiple sclerosis: the plaque and its pathogenesis. N Engl J Med. 2006;354(9):942–55. Babbe H, Roers A, Waisman A, Lassmann H, Goebels N, Hohlfeld R, et al. Clonal expansions of CD8(+) T cells dominate the T cell infiltrate in active multiple sclerosis lesions as shown by micromanipulation and single cell polymerase chain reaction. J Exp Med. 2000;192(3):393–404. Ortiz GG, Pacheco-Moisés FP, Macías-Islas MÁ, Flores-Alvarado LJ, Mireles-Ramírez MA, González-Renovato ED, et al. Role of the blood-brain barrier in multiple sclerosis. Arch Med Res. 2014;45(8):687–97. Kirk S, Frank JA, Karlik S. Angiogenesis in multiple sclerosis: is it good, bad or an epiphenomenon? J Neurol Sci. 2004;217(2):125–30. Lengfeld J, Cutforth T, Agalliu D. The role of angiogenesis in the pathology of multiple sclerosis. Vasc Cell. 2014;6(1):23–6. Holley JE, Newcombe J, Whatmore JL, Gutowski NJ. Increased blood vessel density and endothelial cell proliferation in multiple sclerosis cerebral white matter. Neurosci Lett. 2010;470(1):65–70. Karampoor S, Zahednasab H, Ramagopalan S, Mehrpour M, Keyvani H. Angiogenic factors are associated with multiple sclerosis. J Neuroimmunol. 2016;301:88–93. Argaw AT, Asp L, Zhang J, Navrazhina K, Pham T, Mariani JN, et al. Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease. J Clin Invest. 2012;122(7):2454–68. Argaw AT, Gurfein BT, Zhang Y, Zameer A, John GR. VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown. Proc Natl Acad Sci U S A. 2009;106(6):1977–82. Ali M, Falkenhain K, Njiru BN, Murtaza-Ali M, Ruiz-Uribe NE, Haft-Javaherian M, et al. VEGF signalling causes stalls in brain capillaries and reduces cerebral blood flow in Alzheimer’s mice. Brain. 2022;145(4):1449–63. Weiner HL. Multiple sclerosis is an inflammatory T-cell-mediated autoimmune disease. Arch Neurol. 2004;61(10):1613–5. Szekanecz Z, Koch AE. Mechanisms of disease: angiogenesis in inflammatory diseases. Nat Clin Pract Rheumatol. 2007;3(11):635–43. Croll SD, Ransohoff RM, Cai N, Zhang Q, Martin FJ, Wei T, et al. VEGF-mediated inflammation precedes angiogenesis in adult brain. Exp Neurol. 2004;187(2):388–402. Yoo S-A, Kwok S-K, Kim W-U. Proinflammatory role of vascular endothelial growth factor in the pathogenesis of rheumatoid arthritis: prospects for therapeutic intervention. Mediators Inflamm. 2008;2008:129873. Reinders ME, Sho M, Izawa A, Wang P, Mukhopadhyay D, Koss KE, et al. Proinflammatory functions of vascular endothelial growth factor in alloimmunity. J Clin Invest. 2003;112(11):1655–65. Kouchaki E, Otroshi SB, Faraji S, Nikoueinejad H, Sehat M. The association between vascular endothelial growth factor-related factors and severity of multiple sclerosis. Iran J Allergy Asthma Immunol. 2016 Jun;15(3):204–11. Su JJ, Osoegawa M, Matsuoka T, Minohara M, Tanaka M, Ishizu T, et al. Upregulation of vascular growth factors in multiple sclerosis: correlation with MRI findings. J Neurol Sci. 2006;243(1–2):21–30. Azimi G, Ranjbaran F, Arsang-Jang S, Ghafouri-Fard S, Mazdeh M, Sayad A, et al. Upregulation of VEGF-A and correlation between VEGF-A and FLT-1 expressions in Iranian multiple sclerosis patients. Neurol Sci. 2020;41:1459–65. Proescholdt MA, Jacobson S, Tresser N, Oldfield EH, Merrill MJ. Vascular endothelial growth factor is expressed in multiple sclerosis plaques and can induce inflammatory lesions in experimental allergic encephalomyelitis rats. J Neuropathol Exp Neurol. 2002;61(10):914–25. Kouchaki E, Tamtaji OR, Dadgostar E, Karami M, Nikoueinejad H, Akbari H. Correlation of serum levels of IL-33, IL-37, soluble form of vascular endothelial growth factor receptor 2 (VEGFR2), and circulatory frequency of VEGFR2-expressing cells with multiple sclerosis severity. Iran J Allergy Asthma Immunol. 2017;16(4):329–37. Ogaki A, Ikegaya Y, Koyama R. Vascular abnormalities and the role of vascular endothelial growth factor in the epileptic brain. Front Pharmacol. 2020;11:20. Tremlett H, Yousefi M, Devonshire V, Rieckmann P, Zhao Y. Impact of multiple sclerosis relapses on progression diminishes with time. Neurology. 2009;73(20):1616–23. Article / Publication DetailsFirst-Page Preview
Received: December 21, 2021
Accepted: June 07, 2022
Published online: August 18, 2022
Number of Print Pages: 10
Number of Figures: 6
Number of Tables: 5
ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)
For additional information: https://www.karger.com/NIM
Copyright / Drug Dosage / Disclaimer Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
留言 (0)