ArticlePloS one2015
Heme-Mediated Induction of CXCL10 and Depletion of CD34+ Progenitor Cells Is Toll-Like Receptor 4 Dependent.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Circulating biomarkers associated with pediatric sickle cell disease.Frontiers in molecular biosciences · 2024Article
- Modulation of Heme-Induced Inflammation Using MicroRNA-Loaded Liposomes: Implications for Hemolytic Disorders Such as Malaria and Sickle Cell Disease.International journal of molecular sciences · 2023Article
- Identifying effective diagnostic biomarkers for childhood cerebral malaria in Africa integrating coexpression analysis with machine learning algorithm.European journal of medical research · 2023Article
- Brain endothelial STING1 activation byProceedings of the National Academy of Sciences of the United States of America · 2022Article
- MiR-451a and let-7i-5p loaded extracellular vesicles attenuate heme-induced inflammation in hiPSC-derived endothelial cells.Frontiers in immunology · 2022Article
- Dendritic cell responses to Plasmodium falciparum in a malaria-endemic setting.Malaria journal · 2021Article
- A Computational Approach for Mapping Heme Biology in the Context of Hemolytic Disorders.Frontiers in bioengineering and biotechnology · 2020Article
- Modelling heme-mediated brain injury associated with cerebral malaria in human brain cortical organoids.Scientific reports · 2019Article
- The Glycosylphosphatidylinositol Transamidase Complex Subunit PbGPI16 of Plasmodium berghei Is Important for Inducing Experimental Cerebral Malaria.Infection and immunity · 2018Article
- CCL2 and CXCL10 are associated with poor outcome after intracerebral hemorrhage.Annals of clinical and translational neurology · 2018Article
- Monocyte dysregulation and systemic inflammation during pediatric falciparum malaria.JCI insight · 2017Article
- Article
- Host Biomarkers Are Associated With Response to Therapy and Long-Term Mortality in Pediatric Severe Malaria.Open forum infectious diseases · 2016Article
- Red cell DAMPs and inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Review
- Correction: Heme-Mediated Induction of CXCL10 and Depletion of CD34+ Progenitor Cells Is Toll-Like Receptor 4 Dependent.PloS one · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Plasmodium falciparum infection can cause microvascular dysfunction, cerebral encephalopathy and death if untreated. We have previously shown that high concentrations of free heme, and C-X-C motif chemokine 10 (CXCL10) in sera of malaria patients induce apoptosis in microvascular endothelial and neuronal cells contributing to vascular dysfunction, blood-brain barrier (BBB) damage and mortality. Endothelial progenitor cells (EPC) are microvascular endothelial cell precursors partly responsible for repair and regeneration of damaged BBB endothelium. Studies have shown that EPC's are depleted in severe malaria patients, but the mechanisms mediating this phenomenon are unknown. Toll-like receptors recognize a wide variety of pathogen-associated molecular patterns generated by pathogens such as bacteria and parasites. We tested the hypothesis that EPC depletion during malaria pathogenesis is a function of heme-induced apoptosis mediated by CXCL10 induction and toll-like receptor (TLR) activation. Heme and CXCL10 concentrations in plasma obtained from malaria patients were elevated compared with non-malaria subjects. EPC numbers were significantly decreased in malaria patients (P < 0.02) and TLR4 expression was significantly elevated in vivo. These findings were confirmed in EPC precursors in vitro; where it was determined that heme-induced apoptosis and CXCL10 expression was TLR4-mediated. We conclude that increased serum heme mediates depletion of EPC during malaria pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.