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Hypericin‐induced photosensitization of HeLa cells leads to apoptosis or necrosis
Author(s) -
Vantieghem Annelies,
Assefa Zerihun,
Vandenabeele Peter,
Declercq Wim,
Courtois Stephane,
Vandenheede Jackie R,
Merlevede Wilfried,
de Witte Peter,
Agostinis Patrizia
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01416-1
Subject(s) - hypericin , apoptosis , hela , poly adp ribose polymerase , necrosis , cytochrome c , caspase , programmed cell death , biology , tumor necrosis factor alpha , cytosol , microbiology and biotechnology , cancer research , cell , biochemistry , polymerase , immunology , pharmacology , dna , enzyme , genetics
Here we report that photoactivated hypericin can induce either apoptosis or necrosis in HeLa cells. Under apoptotic conditions the cleavage of poly(ADP‐ribose) polymerase (PARP) into the 85‐kDa product is blocked by the caspase inhibitors benzyloxycarbonyl‐Val‐Ala‐Asp‐fluoromethylketone (z‐VAD‐fmk) and benzyloxycarbonyl‐Asp‐Glu‐Val‐Asp‐fluoromethylketone (z‐DEVD‐fmk). Both inhibitors protect cells from apoptosis but cannot prevent hypericin‐induced necrosis. Conversely, HeLa cells overexpressing the viral cytokine response modifier A (CrmA), which inhibits caspase‐1 and ‐8, still undergo hypericin‐induced apoptosis and necrosis. Evidence is provided for the release of mitochondrial cytochrome c in the cytosol and for procaspase‐3 activation in the hypericin‐induced cell killing.