Exogenous cardiolipin localizes to mitochondria and prevents TAZ knockdown-induced apoptosis in myeloid progenitor cells.

摘要: The concentration and composition of cardiolipin (CL) in mitochondria are altered age-related heart disease, Barth Syndrome, other rare genetic disorders, resulting mitochondrial dysfunction. To explore whether exogenous CL can be delivered to cells, was combined with apolipoprotein A-I generate water-soluble, nanoscale complexes termed nanodisks (ND). Mass spectrometry HL60 myeloid progenitor cell extracts revealed a 30-fold increase cellular content following incubation CL-ND. When CL-ND containing fluorescent analogue employed, confocal microscopy localization mitochondria. ability elicit physiological response examined an culture model Syndrome neutropenia. siRNA knockdown the phospholipid transacylase, tafazzin (TAZ), induced apoptosis these cells. TAZ cells were incubated CL-ND, apoptotic attenuated. Thus, represent potential intervention strategy for replenishment disorders characterized by depletion this key phospholipid.