Ferritin and FasL (CD95L) mediate density dependent apoptosis in primary rat hepatocytes

Journal of Cellular Physiology
Nikolaus BresgenP M Eckl

Abstract

Based on a recent description of an apoptosis stimulating property for hepatocyte derived isoferritins, this investigation demonstrates that ferritin, released in vitro from hepatocytes substantially contributes to density dependent apoptosis in primary hepatocytes and is significantly (P < or = 0.05) inhibited by anti-H-ferritin antibody rH02. Furthermore, total protein release and albumin secretion rapidly decline in a time and density dependent mode under serum-free conditions, whereas ferritin secretion, which is upregulated at initial stages of primary culture is not affected by cell density. Supplementation with dexamethasone (DEX) or proliferative stimulation by epidermal growth factor (EGF) and insulin strongly suppresses density dependent apoptosis. Both regimens have previously been shown to inhibit isoferritin mediated apoptosis in hepatocytes, most likely by interrupting proapotitc mitochondrial signalling. Finally, FasL/Fas also participates in density dependent apoptosis, since apoptosis is significantly (P < or = 0.005) reduced in high density cultures supplemented with an anti-FasL antibody. This antibody has also been shown to neutralise ferritin mediated apoptosis in primary hepatocytes, suggesting a linkage o...Continue Reading

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Citations

Oct 3, 2012·Infection and Immunity·Marybeth LangerJordan Patrick Metcalf
Sep 10, 2013·Archives of Toxicology·Mathieu VinkenVera Rogiers
May 15, 2015·Biomolecules·Nikolaus Bresgen, Peter M Eckl
Mar 12, 2010·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·Qian Yun ZhouLi Ping Zhang
Nov 18, 2008·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·M KhaderP M Eckl
Nov 5, 2014·Antioxidants & Redox Signaling·Giuseppina BarreraFabrizio Gentile

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis