Multiplexed Quantitative Proteomics Reveals Proteomic Alterations in Two Rodent Traumatic Brain Injury Models

In many cases of traumatic brain
injury (TBI), conspicuous
abnormalities,
such as scalp wounds and intracranial hemorrhages, abate over time.
However, many unnoticeable symptoms, including cognitive, emotional,
and behavioral dysfunction, often last from several weeks to years
after trauma, even for mild injuries. Moreover, the cause of such
persistence of symptoms has not been examined extensively. Recent
studies have implicated the dysregulation of the molecular system
in the injured brain, necessitating an in-depth analysis of the proteome
and signaling pathways that mediate the consequences of TBI. Thus,
in this study, the brain proteomes of two TBI models were examined
by quantitative proteomics during the recovery period to determine
the molecular mechanisms of TBI. Our results show that the proteomes
in both TBI models undergo distinct changes. A bioinformatics analysis
demonstrated robust activation and inhibition of signaling pathways
and core proteins that mediate biological processes after brain injury.
These findings can help determine the molecular mechanisms that underlie
the persistent effects of TBI and identify novel targets for drug
interventions.