Modulation of fibronectin expression in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis

Citation
Mca. De-carvalho et al., Modulation of fibronectin expression in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis, BRAZ J MED, 32(5), 1999, pp. 583-592
Citations number
25
Categorie Soggetti
Medical Research General Topics
Journal title
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
ISSN journal
0100879X → ACNP
Volume
32
Issue
5
Year of publication
1999
Pages
583 - 592
Database
ISI
SICI code
0100-879X(199905)32:5<583:MOFEIT>2.0.ZU;2-W
Abstract
Fibronectin (FN), a large family of plasma and extracellular matrix (ECM) g lycoproteins, plays an important role in leukocyte migration. In normal cen tral nervous system (CNS), a fine and delicate mesh of FN is virtually rest ricted to the basal membrane of cerebral blood vessels and to the glial lim itans externa. Experimental autoimmune encephalomyelitis (EAE), an inflamma tory CNS demyelinating disease, was induced in Lewis rats with a spinal cor d homogenate. During the preclinical phase and the onset of the disease, ma rked immunolabelling was observed on the endothelial luminal surface and ba sal lamina of spinal cord and brainstem microvasculature. In the paralytic phase, a discrete labelling was evident in blood vessels of spinal cord and brainstem associated or not with an inflammatory infiltrate. Conversely, i ntense immunolabelling was present in cerebral and cerebellar blood vessels , which were still free from inflammatory cuffs. Shortly after clinical rec overy minimal labelling was observed in a few blood vessels. Brainstem and spinal cord returned to normal, but numerous inflammatory foci and demyelin ation were still evident near the ventricle walls, in the cerebral cortex a nd in the cerebellum. Intense expression of FN in brain vessels ascending f rom the spinal cord towards the encephalon preceded the appearance of infla mmatory cells but faded away after the establishment of the inflammatory cu ff. These results indicate an important role for FN in the pathogenesis of CNS inflammatory demyelinating events occurring during EAE.