Ucci, Valentina (2013) 5-HT2a receptor pathway in oligodendrocyte differentiation: its involvement in Multiple Sclerosis pathogenesis. [Tesi di dottorato]


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Item Type: Tesi di dottorato
Lingua: English
Title: 5-HT2a receptor pathway in oligodendrocyte differentiation: its involvement in Multiple Sclerosis pathogenesis
Ucci, ValentinaUNSPECIFIED
Date: 11 April 2013
Number of Pages: 88
Institution: Università degli Studi di Napoli Federico II
Department: Medicina Molecolare e Biotecnologie Mediche
Scuola di dottorato: Medicina molecolare
Dottorato: Patologia e fisiopatologia molecolare
Ciclo di dottorato: 25
Coordinatore del Corso di dottorato:
Avvedimento, Vittorio Enricoavvedim@unina.it
Santillo, Maria Rosariamarsanti@unina.it
Date: 11 April 2013
Number of Pages: 88
Uncontrolled Keywords: Multiple sclerosis- Differentiation-Oligondedrocytes
Settori scientifico-disciplinari del MIUR: Area 06 - Scienze mediche > MED/04 - Patologia generale
Area 06 - Scienze mediche > MED/09 - Medicina interna
Date Deposited: 11 Apr 2013 14:11
Last Modified: 08 May 2016 01:00
URI: http://www.fedoa.unina.it/id/eprint/9563


Multiple sclerosis (MS) is a chronic demyelinating disease affecting the neurons of brain and spinal cord. In chronic MS lesions oligodendrocytes (the myelin synthesizing cells) precursor cells (OPCs) accumulate with loss of mature OLs, suggesting a differentiation block of OPCs. In MS patients during the active phase of the disease (poussè) the disruption of the blood brain barrier can allow serum antibodies and other molecules to reach the CNS, producing demyelination. Here we demonstrate that IgGs, isolated from MS patients during the acute phase, inhibit PMA-induced differentiation of OPCs by reducing the expression of the OLs differentiation markers in the human OL cell line, MO3-13. In a more specific setting, we found that IgGs from MS patients inhibit differentiation driven by P-ERK activation, The identification of a putative receptor targeted by IgGs present in the biological fluids of MS patients will pave the way to dissect the ERK1/2-dependent signalling pathway leading to demyelination in MS.


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