Effects of Deletion of the Connexin 32 gene on pro and Anti-inflammatories Aspects in the Ethidium Bromide Toxic Demyelination Model

Abstract

Gap junctions are cellular structures that allow transit of molecules between cells, allowing intercellular signaling and transportation. They are formed by proteins denominated connexins and represent key structures in highly complex and integrated tissues, such as the central nervous system (CNS). The present study evaluates the effects of connexin 32 (Cx32) deletion upon CNS inflammation and regeneration/repair after 1, 3, 7, 10 and 20 days after intracerebral injection of ethidium bromide in Cx32 Knock Out and normal mice. To accomplish so, Real Time PCR gene expression quantification was performed upon Tumour Necrosis Factor alpha (TNFα), Transforming Growth Factor beta 1 (TGFβ1), Metalloproteinase 3 (MMP3), Metalloproteinase 9 (MMP9) and Tissue Inhibitor of Metalloproteinases 1 (TIMP1) genes. Results indicate varying differences in the expression pattern, including difference in expression of all evaluated genes in the 3 days post injection period, apex of the acute inflammation mechanisms. These results suggest that Cx32 may perform important functions on molecular, inflammatory and regenerative/repair signalling in the CNS.