Literature DB >> 28250197

Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis.

Marietta Zille1, Saravanan S Karuppagounder1, Yingxin Chen1, Peter J Gough1, John Bertin1, Joshua Finger1, Teresa A Milner1, Elizabeth A Jonas1, Rajiv R Ratan2.   

Abstract

BACKGROUND AND
PURPOSE: Intracerebral hemorrhage leads to disability or death with few established treatments. Adverse outcomes after intracerebral hemorrhage result from irreversible damage to neurons resulting from primary and secondary injury. Secondary injury has been attributed to hemoglobin and its oxidized product hemin from lysed red blood cells. The aim of this study was to identify the underlying cell death mechanisms attributable to secondary injury by hemoglobin and hemin to broaden treatment options.
METHODS: We investigated cell death mechanisms in cultured neurons exposed to hemoglobin or hemin. Chemical inhibitors implicated in all known cell death pathways were used. Identified cell death mechanisms were confirmed using molecular markers and electron microscopy.
RESULTS: Chemical inhibitors of ferroptosis and necroptosis protected against hemoglobin- and hemin-induced toxicity. By contrast, inhibitors of caspase-dependent apoptosis, protein or mRNA synthesis, autophagy, mitophagy, or parthanatos had no effect. Accordingly, molecular markers of ferroptosis and necroptosis were increased after intracerebral hemorrhage in vitro and in vivo. Electron microscopy showed that hemin induced a necrotic phenotype. Necroptosis and ferroptosis inhibitors each abrogated death by >80% and had similar therapeutic windows in vitro.
CONCLUSIONS: Experimental intracerebral hemorrhage shares features of ferroptotic and necroptotic cell death, but not caspase-dependent apoptosis or autophagy. We propose that ferroptosis or necroptotic signaling induced by lysed blood is sufficient to reach a threshold of death that leads to neuronal necrosis and that inhibition of either of these pathways can bring cells below that threshold to survival.
© 2017 American Heart Association, Inc.

Entities:  

Keywords:  apoptosis; cell death; ferroptosis; intracerebral hemorrhage; necrosis

Mesh:

Substances:

Year:  2017        PMID: 28250197      PMCID: PMC5613764          DOI: 10.1161/STROKEAHA.116.015609

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  48 in total

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Review 7.  The Chemical Biology of Ferroptosis in the Central Nervous System.

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Review 8.  Ferroptosis, a Recent Defined Form of Critical Cell Death in Neurological Disorders.

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9.  Cell-specific activation of RIPK1 and MLKL after intracerebral hemorrhage in mice.

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