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- W2022202268 abstract "Background: Mitochondrial inhibition from Ca2+ overload could be of paramount importance to acinar cell fate in pancreatitis. Toxins that cause pancreatitis induce the mitochondrial permeability transition pore (MPTP), but the mechanism and effects of its induction have yet to be determined. We have investigated the role of the MPTP in pancreatic acinar cell injury from bile salts known to cause pancreatitis. Methods: Confocal fluorescence microscopy of isolated murine pancreatic acinar cells was undertaken to measure cytosolic calcium ([Ca2+]c), NAD(P)H autofluorescence (to assess ATP production), mitochondrial membrane potential (Δψm), necrosis (propidium iodide) and apoptosis (caspase:R110-aspartic acid amide). Responses were examined in cells exposed to taurolitholcholic acid 3-sulphate (500 μM TLC-S) with or without MPTP inhibition using either 50 μM bongkrekic acid or 50 μM cyclosporine, or the cytosolic Ca2+ chelator BAPTA. Results: TLC-S induced falls in Δψm and cellular NAD(P)H levels, marked elevation in [Ca2+]c and acinar cell necrosis. Pre-treatment with bongkrekic acid or cyclosporine significantly reduced falls in Δψm, NAD(P)H levels, rises in [Ca2+]c and acinar cell necrosis, but not apoptosis. Pre-treatment with BAPTA prevented these changes. Conclusions: Ca2+ overload induces the MPTP in murine pancreatic acinar cells, which significantly impairs mitochondrial function and is a major cause of pancreatic acinar cell necrosis from toxins that induce acute pancreatitis." @default.
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- W2022202268 date "2008-11-01" @default.
- W2022202268 modified "2023-09-25" @default.
- W2022202268 title "PANCREATIC ACINAR CELL NECROSIS FROM CA2+ OVERLOAD DEPENDS ON THE MITOCHONDRIAL PERMEABILITY TRANSITION PORE" @default.
- W2022202268 doi "https://doi.org/10.1097/01.mpa.0000335344.73826.3b" @default.
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