BioProject

The pathophysiology of TBI is complex and can be divided into primary damage resulting from mechanical impact and secondary damage, which comprises complex interconnecting structural, functional, cellular and molecular changes. More...

The pathophysiology of TBI is complex and can be divided into primary damage resulting from mechanical impact and secondary damage, which comprises complex interconnecting structural, functional, cellular and molecular changes. The current study was performed to evaluate gene expression profiles in the frontal cortex at 1 month, a time at which secondary damaged can be detected, following lateral fluid percussion induced TBI (lfp-TBI) and rotational acceleration induced TBI (rot-TBI) in rats. After lfp-TBI, genes significantly expressed belong to metabolic process, immune system, cellular process, and morphogenesis. After rot-TBI, genes were related to apoptosis response, morphogenesis, angiogenesis, extracellular matrix, metabolic process, and transport and localization. Interestingly, we found that the molecular signature of secondary TBI share similar alterations to pathologies related to ischemia stroke and depression. Overlapped genes belong to immune/inflammation processes, extracellular organization, and intracellular trafficking. Their biological implications in multiple brain pathologies remain to be further examined. Nonetheless, these genes homologies may indicate that therapeutic strategies following stroke and depression may also be beneficial after trauma. Overall design: Two rat models of trauma were used: lateral fluid percussion injury (N=3) and head acceleration rotational injury (N=3). Total RNA was extracted from frontal cortex 1 month after trauma. Trauma rats were compared to sham rats. Sham animals were subjected to anesthesia and all surgery but were not subjected to trauma. Less...