Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects
| Autor: | Alberto Hernández, Francisco Coret-Ferrer, Deepali Mathur, Bonaventura Casanova, Eva María-Lafuente, Lucas Sorribes, Juan R. Ureña-Peralta, Gerardo López-Rodas, Maria Burgal-Marti |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty glucose metabolism neuromyelitis optica Biology multiple sclerosis Article cerebrospinal fluid lcsh:RC321-571 03 medical and health sciences Myelin 0302 clinical medicine Cerebrospinal fluid Downregulation and upregulation Gene expression medicine Remyelination Axon lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry gene expression Neuromyelitis optica General Neuroscience Multiple sclerosis medicine.disease 030104 developmental biology medicine.anatomical_structure nervous system 030217 neurology & neurosurgery |
| Zdroj: | Brain Sciences r-IIS La Fe. Repositorio Institucional de Producción Científica del Instituto de Investigación Sanitaria La Fe instname Brain Sciences; Volume 8; Issue 1; Pages: 1 r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA Brain Sciences, Vol 8, Iss 1, p 1 (2017) r-CIPF: Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF) Centro de Investigación Principe Felipe (CIPF) r-CIPF. Repositorio Institucional Producción Científica del Centro de Investigación Principe Felipe (CIPF) |
| ISSN: | 2076-3425 |
| Popis: | Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate the pathophysiological mechanisms underpinning axonal injury through hitherto unknown factors present in cerebrospinal fluid (CSF) that may regulate axonal damage, remyelinate the axon and make functional recovery possible. We employed primary cultures of rat unmyelinated cerebellar granule neurons and treated them with CSF obtained from MS and Neuromyelitis optica (NMO) patients. We performed microarray gene expression profiling to study changes in gene expression in treated neurons as compared to controls. Additionally, we determined the influence of gene-gene interaction upon the whole metabolic network in our experimental conditions using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) program. Our findings revealed the downregulated expression of genes involved in glucose metabolism in MS-derived CSF-treated neurons and upregulated expression of genes in NMO-derived CSF-treated neurons. We conclude that factors in the CSF of these patients caused a perturbation in metabolic gene(s) expression and suggest that MS appears to be linked with metabolic deformity. |
| Databáze: | OpenAIRE |
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