Key result
Bid deficiency in mice reduces early brain lesion volume ~30% without improving long-term functional outcomes.
Why the study?
Bid is a proapoptotic protein hypothesized to contribute to cell death and functional outcome after traumatic brain injury, but its role was not fully understood.
Does Bid deficiency reduce cell death and improve functional outcome after traumatic brain injury in mice?
Does Bid deficiency reduce cell death and improve functional outcome after traumatic brain injury in mice?
Absolute Event Rate: 5.9% vs 8.4%
p-value: p=<0.001
Bid deficiency in mice reduces early posttraumatic brain cell death and tissue damage but does not improve long-term functional outcomes after controlled cortical impact.
Bid inhibition may limit acute cell death after experimental TBI; leaves open clinical translation.
Bid is a proapoptotic member of the Bcl-2 family that mediates cell death by caspase-dependent and -independent pathways. We tested mice genetically deficient in Bid in a controlled cortical impact (CCI) model to examine the hypothesis that Bid contributes to cell death and functional outcome after traumatic brain injury. After CCI, truncated Bid (15 kDa) was robustly detected in cortical brain homogenates of wild-type mice. Bid-/- mice had decreased numbers of cortical cells with acute plasmalemma injury at 6 h (wild type (WT), 1721+/-124; Bid-/-, 1173+/-129 cells/ x 200 field; P<0.01), decreased numbers of cells expressing cleaved caspase-3 in the dentate gyrus at 48 h (WT, 113+/-15; Bid-/-, 65+/-9 cells/ x 200 field; P<0.05), and reduced lesion volume at 12 days (Bid-/-, 5.9+/-0.4 mm(3); WT, 8.4+/-0.4 mm(3); P<0.001), but did not differ from WT mice at later times after injury regarding lesion size (30 days) or brain tissue atrophy (40 days). Compared with naïve mice, injured mice in both groups performed significantly worse on motor and Morris water maze (MWM) tests; however, mice deficient in Bid did not differ from WT in postinjury motor and MWM performance. The data show that Bid deficiency decreases early posttraumatic brain cell death and tissue damage, but does not reduce functional outcome deficits after CCI in mice.
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Bermpohl et al. (2006) studied Traumatic Brain Injury. Bid deficiency (Bid-/-) vs. Wild-type (WT) mice was evaluated on Lesion volume at 12 days (p=<0.001). Bid deficiency in mice decreased early posttraumatic brain lesion volume at 12 days (5.9 vs 8.4 mm3; P<0.001) but did not improve long-term functional outcomes after controlled cortical impact.
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