Key result
Coexpression of the novel hypoxia-inducible spliced variant Bnip3Δex3 (8.2-kDa) inhibited widespread cell death triggered by full-length Bnip3 (26-kDa) in ventricular myocytes.
Population
Postnatal ventricular myocytes and Bnip3(-/-) mouse embryonic fibroblasts
Comparison
Alternative splicing of Bnip3 to Bnip3Δex3… vs Control cells without Bnip3Δex3 coexpression or…
Design
Preclinical
Authors
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Bnip3Δex3 may confer intrinsic protection against hypoxic myocyte death; leaves open its therapeutic relevance in human ischemia.
A novel spliced variant of Bnip3 (Bnip3Δex3) acts as an intrinsic defense mechanism against hypoxia-induced mitochondrial defects and cell death in ventricular myocytes.
Gang et al. (2011) studied Hypoxia/ischemic stress in ventricular myocytes. Bnip3Δex3 coexpression vs. Bnip3FL alone was evaluated on Cell death and mitochondrial localization. Coexpression of the novel hypoxia-inducible spliced variant Bnip3Δex3 (8.2-kDa) inhibited widespread cell death triggered by full-length Bnip3 (26-kDa) in ventricular myocytes.
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