Plasmodium falciparum picks (on) EPCR

Aird, William C.; Mosnier, Laurent O.; Fairhurst, Rick M.

doi:10.1182/blood-2013-09-521005

Cited by 40 publications

(41 citation statements)

References 30 publications

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“…6 Recently, additional hemostatic abnormalities have been identified including a reduction of VWF-cleaving protease, ADAMTS13, 7 in plasma and a loss of endothelial protein C receptor (EPCR) in the cerebral vessels in patients with cerebral malaria. 8 One other historical observation is of interest: severe P falciparum cerebral malaria is less common in blood group O individuals, 9 and this finding holds up even with more recent genome-wide association studies. In addition, VWF levels are 25% to 30% higher in non-O blood groups, 10 which might suggest an association for VWF levels in the pathogenesis of cerebral malaria.…”

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confidence: 86%

“…The latter assumption does not necessarily preclude them from mediating biological effects outside of platelets. Indeed, circRNAs may still play a role in other cells, as shown previously for mRNAs and miRNAs, 8 provided that they are expelled within exosomes or larger microparticles, under basal conditions or upon activation, which remains to be seen. Because exon-intron circRNAs regulate transcription in nucleated cells, 9 it is tempting to speculate that circRNAs that accumulate in platelets may end up regulating gene expression and function of other recipient cells of the circulatory system.…”

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confidence: 92%

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The heads and the tails of malaria and VWF

Montgomery

2016

Blood

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confidence: 86%

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confidence: 92%

The heads and the tails of malaria and VWF

Montgomery

2016

Blood

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“…They also provide a rationale for the development of novel therapeutic strategies based on soluble EPCR and EPCR ligands (refer to the original articles and subsequent comment/review articles for further discussion on this [92][93][94] ). The addition of soluble EPCR at levels between 15 and 300 ng/mL was shown to progressively inhibit the binding between DC8-expressing parasites and endothelial cells.…”

Section: Org Frommentioning

confidence: 99%

Endothelial cell protein C receptor: a multiliganded and multifunctional receptor

Rao

Esmon

Pendurthi

2014

Blood

168

109

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Endothelial cell protein C receptor (EPCR) was first identified and isolated as a cellular receptor for protein C on endothelial cells. EPCR plays a crucial role in the protein C anticoagulant pathway by promoting protein C activation. In the last decade, EPCR has received wide attention after it was discovered to play a key role in mediating activated protein C (APC)-induced cytoprotective effects, including antiapoptotic, anti-inflammatory, and barrier stabilization. APC elicits cytoprotective signaling through activation of protease activated receptor-1 (PAR1). Understanding how EPCR-APC induces cytoprotective effects through activation of PAR1, whose activation by thrombin is known to induce a proinflammatory response, has become a major research focus in the field. Recent studies also discovered additional ligands for EPCR, which include factor VIIa, Plasmodium falciparum erythrocyte membrane protein, and a specific variant of the T-cell receptor. These observations open unsuspected new roles for EPCR in hemostasis, malaria pathogenesis, innate immunity, and cancer. Future research on these new discoveries will undoubtedly expand our understanding of the role of EPCR in normal physiology and disease, as well as provide novel insights into mechanisms for EPCR multifunctionality. Comprehensive understanding of EPCR may lead to development of novel therapeutic modalities in treating hemophilia, inflammation, cerebral malaria, and cancer.

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“…During the symptomatic phase of malaria several clinical complications can occur and are defined as severe malaria. These complications are anemia, cerebral malaria, placental malaria, and acute lung injury/acute respiratory distress syndrome (ALI/ARDS) [3]. The ALI/ARDS has been diagnosed in patients suffering from malaria caused by all the species that cause disease in humans, including P. knowlesi [4]; however it is more common in P. falciparum and P. vivax malaria [5].…”

Section: Introductionmentioning

confidence: 99%

Association of Heme Oxygenase 1 with Lung Protection in Malaria-Associated ALI/ARDS

Pereira

Ortolan

Sercundes

et al. 2016

Mediators of Inflammation

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Malaria is a serious disease, caused by the parasite of the genus Plasmodium, which was responsible for 440,000 deaths in 2015. Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is one of the main clinical complications in severe malaria. The murine model DBA/2 reproduces the clinical signs of ALI/ARDS in humans, when infected with Plasmodium berghei ANKA. High levels of HO-1 were reported in cases of severe malaria. Our data indicated that the HO-1 mRNA and protein expression are increased in mice that develop malaria-associated ALI/ARDS (MA-ALI/ARDS). Additionally, the hemin, a HO-1 inducing drug, prevented mice from developing MA-ALI/ARDS when administered prior to the development of MA-ALI/ARDS in this model. Also, hemin treatment showed an amelioration of respiratory parameters in mice, high VEGF levels in the sera, and a decrease in vascular permeability in the lung, which are signs of ALI/ARDS. Therefore, the induction of HO-1 before the development of MA-ALI/ARDS could be protective. However, the increased expression of HO-1 on the onset of MA-ALI/ARDS development may represent an effort to revert the phenotype of this syndrome by the host. We therefore confirm that HO-1 inducing drugs could be used for prevention of MA-ALI/ARDS in humans.

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Plasmodium falciparum picks (on) EPCR

Cited by 40 publications

References 30 publications

The heads and the tails of malaria and VWF

The heads and the tails of malaria and VWF

Endothelial cell protein C receptor: a multiliganded and multifunctional receptor

Association of Heme Oxygenase 1 with Lung Protection in Malaria-Associated ALI/ARDS

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