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Upregulation of VEGF-A and correlation between VEGF-A and FLT-1 expressions in Iranian multiple sclerosis patients

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Abstract

Multiple sclerosis (MS) is among the most common diseases affecting brain and spinal cord. MS progression is characterized by breakdown of blood brain barrier which leads to increased vascular permeability and angiogenesis. Consequently, vascular endothelial growth factor A (VEGF) and its receptors are considered to be important components of MS progression. VEGFA and fms-related tyrosine kinase 1 (FLT1) play important roles in various aspects of MS. In this study, we investigated the relationship between these genes and MS. For this purpose, the expression levels of VEGFA and FLT1 were measured in the blood of 50 relapsing-remitting MS (RR-MS) patients and 50 healthy individuals using TaqMan quantitative real-time PCR. A significant upregulation of VEGFA expression was observed among MS patients compared with controls (p = 0.04). However, the difference in FLT1 gene expression between study groups was insignificant (p = 0.947). In addition, there was a significant positive correlation between VEGFA and FLT1 genes expressions (r = 0.769, p < 0.0001). In spite of the highly complex molecular mechanisms behind this, the findings imply participation of VEGFA in the pathogenesis of MS.

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Funding

The current study was supported by a grant (grant number 9296) from Shahid Beheshti University of Medical Sciences.

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Correspondence to Arezou Sayad or Mohammad Taheri.

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The study was approved by the local Ethics Committee of Shahid Beheshti University of Medical Sciences (SBMU Academic Ethics Committee on Biomedical Research). To be included in the study, all patients and controls were asked to sign an informed consent form and the blood samples were collected at Iran MS Society Clinic.

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The authors declare that they have no conflict of interest.

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Azimi, G., Ranjbaran, F., Arsang-Jang, S. et al. Upregulation of VEGF-A and correlation between VEGF-A and FLT-1 expressions in Iranian multiple sclerosis patients. Neurol Sci 41, 1459–1465 (2020). https://doi.org/10.1007/s10072-019-04234-2

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  • DOI: https://doi.org/10.1007/s10072-019-04234-2

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