posted on 2023-12-14, 19:38authored byDiego Iacono, Kathleen Hatch, Erin K. Murphy, Robert N. Cole, Jeremy Post, Fabio Leonessa, Daniel P. Perl
Repeated blast-traumatic brain injury (blast-TBI) has
been hypothesized
to cause persistent and unusual neurological and psychiatric symptoms
in service members returning from war zones. Blast-wave primary effects
have been supposed to induce damage and molecular alterations in the
brain. However, the mechanisms through which the primary effect of
an explosive-driven blast wave generate brain lesions and induce
brain consequences are incompletely known. Prior findings from rat
brains exposed to two consecutive explosive-driven blasts showed molecular
changes (hyperphosphorylated-Tau, AQP4, S100β, PDGF, and DNA-polymerase-β)
that varied in magnitude and direction across different brain regions.
We aimed to compare, in an unbiased manner, the proteomic profile
in the hippocampus of double blast vs sham rats using mass spectrometry
(MS). Data showed differences in up- and down-regulation for protein
abundances in the hippocampus of double blast vs sham rats. Tandem
mass tag (TMT)-MS results showed 136 up-regulated and 94 down-regulated
proteins between the two groups (10.25345/C52B8VP0X). These TMT-MS findings revealed changes never described before
in blast studies, such as increases in MAGI3, a scaffolding protein
at cell–cell junctions, which were confirmed by Western blotting
analyses. Due to the absence of behavioral and obvious histopathological
changes as described in our previous publications, these proteomic
data further support the existence of an asymptomatic blast-induced
molecular altered status (ABIMAS) associated with specific protein
changes in the hippocampus of rats repeatedly expsosed to blast waves
generated by explosive-driven detonations.