Absence of galectin-3 attenuates neuroinflammation improving functional recovery after spinal cord injury.

Abstract

After spinal cord injury (SCI), a cascade of events begins. At first, there is physical damage with disruption of the blood-brain barrier (BBB) and the integrity of the nervous tissue. The disruption of central nervous system (CNS) BBB alters the endothelial permeability, the protein and chemokines expression and the propensity to release in situ inflammatory cytokines, overcoming anti-inflammatory signals, facilitating the attraction and entry of immune system cells into the injured spinal cord parenchyma (Gaudet et al., 2011). As a result, there is a neuroinflammatory response with changes in blood flow, edema, cell infiltration, apoptosis and release of axonal growth inhibitory factors. Nerve function loss occurs when the nerve impulse propagation is interrupted and do not reach its target. This disorder encompasses neuron and glia apoptosis, accompanied by Wallerian degeneration of disconnected axons, and CNS cells exposure to a hostile microenvironment that hampers axon regeneration (Mautes et al., 2000; Harkey et al., 2003). Additionally, the damage spreads further in a phenomenon called progressive hemorrhagic necrosis – PHN, with the appearance of petechial hemorrhagic foci and deterioration in areas outside the lesion epicenter during the next 2 – 24 hours after the trauma (Simard et al., 2007). Our laboratory investigates the role of galectin-3, a protein linked to mechanisms of inflammation, behind the cellular mechanisms of neural degeneration/regeneration with perspectives of a novel treatment (Mostacada et al., 2015).