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• W2076420512 abstract "In the genetic disease cystic fibrosis (CF), the most common mutation F508del promotes the endoplasmic reticulum (ER) retention of misfolded CF proteins. Furthermore, in homozygous F508del-CFTR airway epithelial cells, the histamine Ca2+ mobilization is abnormally increased. Because the uptake of Ca2+ by mitochondria during Ca2+ influx or Ca2+ release from ER stores may be crucial for maintaining a normal Ca2+ homeostasis, we compared the mitochondria morphology and distribution by transmission electron microscopy technique and the mitochondria membrane potential variation (ΔΨmit) using a fluorescent probe (TMRE) on human CF (CF-KM4) and non-CF (MM39) tracheal serous gland cell lines. Confocal imaging of Rhod-2–AM-loaded or of the mitochondrial targeted cameleon 4mtD3cpv-transfected human CF and non-CF cells, were used to examine the ability of mitochondria to sequester intracellular Ca2+. The present study reveals that (i) the mitochondria network is fragmented in F508del-CFTR cells, (ii) the ΔΨmit of CF mitochondria is depolarized compared non-CF mitochondria, and (iii) the CF mitochondria Ca2+ uptake is reduced compared non-CF cells. We propose that these defects in airway epithelial F508del-CFTR cells are the consequence of mitochondrial membrane depolarization leading to a deficient mitochondrial Ca2+ uptake." @default.
• W2076420512 created "2016-06-24" @default.
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• W2076420512 date "2009-07-01" @default.
• W2076420512 modified "2023-09-25" @default.
• W2076420512 title "Dysfunction of mitochondria Ca2+ uptake in cystic fibrosis airway epithelial cells" @default.
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• W2076420512 doi "https://doi.org/10.1016/j.mito.2009.02.003" @default.
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