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Spatial transcriptome analysis defines heme as a hemopexin-targetable inflammatoxin in the brain

ABSTRACT: Spatial transcriptome analysis defines heme as a hemopexin-targetable inflammatoxin in the brain

PROVIDER: PRJNA754793 | ENA |

REPOSITORIES: ENA

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Spatial transcriptome analysis defines heme as a hemopexin-targetable inflammatoxin in the brain

Project description:After intracranial hemorrhages, heme is released from cell-free hemoglobin. This red blood cell toxin may drive secondary brain injury at the hematoma-brain interface. This study aimed to generate a spatially resolved map of the transcriptome-wide gene expression changes in the heme-exposed brain and define the potential therapeutic activity of the heme-binding protein hemopexin.

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Haptoglobin and Hemopexin Redirect Heme-Driven Oxidative Stress and Neurotoxicity in Organotypic Brain Slices

Project description:The mechanistic links between hemoglobin oxidation, heme release, and neuronal death after intracerebral hemorrhage are incompletely defined. Using organotypic brain-slice cultures (BSCs) that model the RBC-toxin cascade, we dissect how the scavenger proteins haptoglobin (Hp) and hemopexin (Hpx) interrupt this pathology. BSCs exposed to free hemoglobin, heme, or their complexes (HbHp, hemeHpx) reveal that both Hb and heme drive iron-dependent neuronal injury, while Hp and Hpx confer protection by distinct mechanisms. Multi-modal readouts – including iron quantification, lipid peroxidation, neuronal apoptosis, and RNA-seq – demonstrate that Hpx abolishes toxicity by sequestering heme, whereas Hp stabilizes Hb and enables Nrf2-dependent cytoprotective gene expression. These data quantitatively map how Hp and Hpx reroute hemolytic toxicity toward resilience.

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Targeting Circulating Labile Heme as a Defense Strategy Against Malaria

Project description:Severe presentations of malaria emerge as parasites from Plasmodium spp. proliferate and lyse red blood cells (RBC), producing extracellular hemoglobin (HB). The heme prosthetic groups are released upon HB oxidation generating circulating labile heme. Here we asked whether scavenging of extracellular HB and/or labile heme, by haptoglobin (HP) and/or hemopexin (HPX), respectively, is protective against severe presentations of malaria. We found that circulating labile heme is an independent risk factor for cerebral and non-cerebral severe presentations of P. falciparum malaria. Labile heme was negatively correlated with HP and HPX, which were however, not risk factors for severe P. falciparum malaria. Genetic HP and/or HPX deletion in mice led to accumulation of labile heme in plasma and kidneys in response to Plasmodium (chabaudi chabaudi) infection. This was associated with increased mortality and acute kidney injury (AKI) in ageing but not adult mice, corroborated in P. falciparum malaria by a an inverse correlation between HPX and heme with serological markers of AKI. In conclusion, HP and HPX exert an age-dependent protective effect against malaria that counters the pathogenesis of AKI in mice and presumably in humans.

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Haptoglobin and Hemopexin Redirect Heme-Driven Oxidative Stress and Neurotoxicity in Organotypic Brain Slices

Project description:Haptoglobin and Hemopexin Redirect Heme-Driven Oxidative Stress and Neurotoxicity in Organotypic Brain Slices

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Reciprocal gene editing defines targetable mutant H3.3 oncohistone effectors in pediatric glioma

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Microarray identification of functional modules involving Haptoglobin and/or Hemopexin

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The covariance environment defines cellular niches for spatial inference

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Hemin-induced DEGs in Lung, Kidney of WT and hepatic SR-BI KO mice

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