Effect of IGF-1 gene therapy in the inflammatory response of microglia in a traumatic brain injury model

HERRERA, MACARENA LORENA; FALOMIR-LOCKHART, EUGENIA; MARCHESE, NATALIA; DOLCETTI, FRANCO JUAN CRUZ; GARCÍA-SEGURA, LUIS MIGUEL; HEREÑU, CLAUDIA B.; BELLINI, MARIA JOSE

Buenos Aires

Congreso; 2nd FALAN Congress; 2016

Sociedad Argentina de Neurociencias (SAN)

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. Neuroinflammation is well established as a key secondary injury mechanism after TBI, and contributes to the activation of glial cells and the release of pro-inflammatory cytokines and chemokines. Such activation it is mainly regulated by microglia and astroglia. Neurotrophic factors like the insulin-like growth factor-I (IGF-I) exerts neuroprotective actions that are mediated at least in part by control of activation of glia. OBJECTIVE: In this study we have assessed the efficacy of IGF-I gene therapy in reducing the inflammatory response of microglia after a stab wound injury. METHODS: Wistar male rats were divided into 3 experimental groups: G1: injected IP with RAd- HD-IGF-1, G2: injected IP with Rad-HD-GFP and G3: control with PBS, fourteen days previous to stab wound injury in the cortex. Two days after injury rats were sacrificed and gliosis was assessed by immunohistochemistry. The number of Iba I immunoreactive microglia were estimated in the cortex within a distance of 0- 1252,5um from the wound border, divided into five consecutives frames of 250,5x835,52um2. In addition, Iba I-positive cells were classified in two morphological phenotypes: reactive and nonreactive