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The BH3 interacting-domain death agonist (BID) is a pro-apoptotic member of the Bcl-2 protein family. While proteolytic processing of BID links death receptor-induced apoptosis to the mitochondrial apoptosis pathway, we previously showed that full length BID also translocates to mitochondria during Ca 2+ -induced neuronal cell death. Moreover, mitochondrial carrier homolog 2 (MTCH2) was identified as a mitochondrial protein that interacts with BID during cell death. We started our studies by investigating the effect of  Mtch2  silencing in a well-established model of Ca 2+ -induced mitochondrial permeability transition pore opening in non-neuronal HCT116 cells. We found that silencing of  Mtch2  inhibited mitochondrial swelling and the associated decrease in mitochondrial energetics, suggesting a pro-death function for MTCH2 during Ca 2+ -induced injury. Next, we explored the role of BID and MTCH2 in mediating Ca 2+ -induced injury in primary cortical neurons triggered by prolonged activation of NMDA glutamate receptors. Analysis of intracellular Ca 2+  transients, using time-lapse confocal microscopy, revealed that neurons lacking  Bid  showed markedly reduced Ca 2+  levels during the NMDA excitation period. These Ca 2+  transients were further decreased when  Mtch2  was also silenced. Collectively, our data suggest that BID and MTCH2 functionally interact to promote Ca 2+ -induced neuronal injury.

Mitochondrial Carrier Homolog 2 Functionally Co-operates With BH3 Interacting-Domain Death Agonist in Promoting Ca2+-Induced Neuronal Injury