Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/1536
Title: Activity, but not mRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis
Authors: Petković, F.
Živanović, J.
Blaževski, J.
Timotijević, G.
Momčilović, M.
Stanojević, T.
Stamenković, V. 
Milošević, V.
Stojković, M. Mostarica
Miljković, D.
Keywords: Experimental autoimmune encephalomyelitis;Gelatinase;Matrix metalloproteinase;Neuroinflammation;Rat
Issue Date: 1-Apr-2015
Journal: Neuroscience
Abstract: 
© 2015 IBRO. Experimental autoimmune encephalomyelitis (EAE) is a model of multiple sclerosis (MS), inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS). Clinically manifested EAE can be induced in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats by immunization with spinal cord homogenate (SCH) and complete Freund's adjuvant (CFA). Matrix metalloproteinases (MMP) play important roles in various steps of MS and EAE pathogenesis. Expression of gelatinases MMP2 and MMP9, their activator MMP14 and their inhibitor tissue inhibitor of MMP (TIMP)1 in the CNS of AO and DA rats immunized with SCH. +. CFA was determined. Expression of mRNA for MMP2, MMP9 and MMP14 was higher and expression of TIMP1 mRNA was lower in AO rats. However, gelatinase activity in spinal cords was higher in samples obtained from DA rats. Further, while there was no strain difference in MMP2 and MMP9 mRNA expression in lymph nodes of the immunized rats, gelatinase activity was higher in DA rats. This activity was reduced by antiinflammatory cytokines interleukin (IL)-10 and IL-4. Interestingly, gelatinase activity was detected in the nuclei of cells within the CNS, but not of those in lymph nodes. Our results imply that posttranscriptional regulation of MMP2 and MMP9 expression and/or function determines low gelatinase activity within the CNS and in immune cells of EAE-resistant AO rats.
URI: https://biore.bio.bg.ac.rs/handle/123456789/1536
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2015.02.015
Appears in Collections:Journal Article

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