ArticlePloS one2011
Platelets alter gene expression profile in human brain endothelial cells in an in vitro model of cerebral malaria.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- A novel minimally-invasive method to sample human endothelial cells for molecular profiling.PloS one · 2015Trial
- Cerebral Malaria and Neuronal Implications of Plasmodium Falciparum Infection: From Mechanisms to Advanced Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Platelet disturbances correlate with endothelial cell activation in uncomplicated Plasmodium vivax malaria.PLoS neglected tropical diseases · 2020Article
- Identification of Methylated Gene Biomarkers in Patients with Alzheimer's Disease Based on Machine Learning.BioMed research international · 2020Article
- Gene expression profiling in blood from cerebral malaria patients and mild malaria patients living in Senegal.BMC medical genomics · 2019Article
- Article
- Neuro-Immune Hemostasis: Homeostasis and Diseases in the Central Nervous System.Frontiers in cellular neuroscience · 2018Review
- Cerebral malaria--clinical manifestations and pathogenesis.Metabolic brain disease · 2016Review
- Molecular basis of human cerebral malaria development.Tropical medicine and health · 2016Review
- FAM19A4 is a novel cytokine ligand of formyl peptide receptor 1 (FPR1) and is able to promote the migration and phagocytosis of macrophages.Cellular & molecular immunology · 2015Article
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- Experimental Models of Microvascular Immunopathology: The Example of Cerebral Malaria.Journal of neuroinfectious diseases · 2014Article
- Dissecting gene expression at the blood-brain barrier.Frontiers in neuroscience · 2014Review
- Endothelial cells potentiate interferon-γ production in a novel tripartite culture model of human cerebral malaria.PloS one · 2013Article
- A potential role for plasma uric acid in the endothelial pathology of Plasmodium falciparum malaria.PloS one · 2013Article
- Intracellular proteolysis of kininogen by malaria parasites promotes release of active kinins.Malaria journal · 2012Article
- Plasma levels of angiopoietin-1 and -2 predict cerebral malaria outcome in Central India.Malaria journal · 2011Article
- Malaria: modification of the red blood cell and consequences in the human host.British journal of haematology · 2011Review
- Translating cell survival and cell longevity into treatment strategies with SIRT1.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · 2011Review
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet adhesion to the brain microvasculature has been associated with cerebral malaria (CM) in humans, suggesting that platelets play a role in the pathogenesis of this syndrome. In vitro co-cultures have shown that platelets can act as a bridge between Plasmodium falciparum-infected red blood cells (pRBC) and human brain microvascular endothelial cells (HBEC) and potentiate HBEC apoptosis. Using cDNA microarray technology, we analyzed transcriptional changes of HBEC in response to platelets in the presence or the absence of tumor necrosis factor (TNF) and pRBC, which have been reported to alter gene expression in endothelial cells. Using a rigorous statistical approach with multiple test corrections, we showed a significant effect of platelets on gene expression in HBEC. We also detected a strong effect of TNF, whereas there was no transcriptional change induced specifically by pRBC. Nevertheless, a global ANOVA and a two-way ANOVA suggested that pRBC acted in interaction with platelets and TNF to alter gene expression in HBEC. The expression of selected genes was validated by RT-qPCR. The analysis of gene functional annotation indicated that platelets induce the expression of genes involved in inflammation and apoptosis, such as genes involved in chemokine-, TREM1-, cytokine-, IL10-, TGFβ-, death-receptor-, and apoptosis-signaling. Overall, our results support the hypothesis that platelets play a pathogenic role in CM.
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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.