Traumatic Brain Injury in Mice Deficient in Bid: Effects on Histopathology and Functional Outcome
作者： Daniela Bermpohl , Zerong You , Stanley J Korsmeyer , Michael A Moskowitz , Michael J Whalen
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摘要: 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 controlled cortical impact (CCI) model to examine hypothesis contributes functional outcome after traumatic brain injury. After CCI, truncated (15 kDa) was robustly detected homogenates wild-type mice. Bid-/- had decreased numbers cells with acute plasmalemma injury at 6 h (wild type (WT), 1721+/-124; Bid-/-, 1173+/-129 cells/ x 200 field; P<0.01), expressing cleaved caspase-3 dentate gyrus 48 (WT, 113+/-15; 65+/-9 P<0.05), reduced lesion volume 12 days (Bid-/-, 5.9+/-0.4 mm(3); WT, 8.4+/-0.4 P<0.001), but did not differ from WT later times regarding size (30 days) or tissue atrophy (40 days). Compared naive mice, injured both groups performed significantly worse on motor Morris water maze (MWM) tests; however, postinjury MWM performance. The data show deficiency decreases early posttraumatic damage, does reduce deficits CCI
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