ArticleFrontiers in immunology2014
Systemic and Cerebral Vascular Endothelial Growth Factor Levels Increase in Murine Cerebral Malaria along with Increased Calpain and Caspase Activity and Can be Reduced by Erythropoietin Treatment.
Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- A comprehensive rhythmicity analysis of host proteins and immune factors involved in malaria pathogenesis to decipher the importance of host circadian clock in malaria.Frontiers in immunology · 2023Article
- Article
- Binding of Plasmodium falciparum to CD36 can be shielded by the glycocalyx.Malaria journal · 2017Article
- Expanding the antimalarial toolkit: Targeting host-parasite interactions.The Journal of experimental medicine · 2016Review
- Erythropoietin Slows Photoreceptor Cell Death in a Mouse Model of Autosomal Dominant Retinitis Pigmentosa.PloS one · 2016Article
- VEGF: inflammatory paradoxes.Pathogens and global health · 2015Article
- Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria.PLoS pathogens · 2015Article
- Increased CD11b and Hypoxia-Inducible Factors-1alpha Expressions in the Lung Tissue and Surfactant Protein-D Levels in Serum Are Related with Acute Lung Injury in Severe Malaria of C57BL/6 Mice.Iranian journal of parasitologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of cerebral malaria (CM) includes compromised microvascular perfusion, increased inflammation, cytoadhesion, and endothelial activation. These events cause blood-brain barrier disruption and neuropathology and associations with the vascular endothelial growth factor (VEGF) signaling pathway have been shown. We studied this pathway in mice infected with Plasmodium berghei ANKA causing murine CM with or without the use of erythropoietin (EPO) as adjunct therapy. ELISA and western blotting was used for quantification of VEGF and relevant proteins in brain and plasma. CM increased levels of VEGF in brain and plasma and decreased plasma levels of soluble VEGF receptor 2. EPO treatment normalized VEGF receptor 2 levels and reduced brain VEGF levels. Hypoxia-inducible factor (HIF)-1α was significantly upregulated whereas cerebral HIF-2α and EPO levels remained unchanged. Furthermore, we noticed increased caspase-3 and calpain activity in terminally ill mice, as measured by protease-specific cleavage of α-spectrin and p35. In conclusion, we detected increased cerebral and systemic VEGF as well as HIF-1α, which in the brain were reduced to normal in EPO-treated mice. Also caspase and calpain activity was reduced markedly in EPO-treated mice.
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