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Statements

Subject Item
n2:RIV%2F60077344%3A_____%2F14%3A00435190%21RIV15-GA0-60077344
rdf:type
skos:Concept n15:Vysledek
dcterms:description
Background: Invasion of mosquito salivary glands (SGs) by Plasmodium falciparum sporozoites is an essential step in the malaria life cycle. How infection modulates gene expression, and affects hematophagy remains unclear. Principal Findings: Using Affimetrix chip microarray, we found that at least 43 genes are differentially expressed in the glands of Plasmodium falciparum-infected Anopheles gambiae mosquitoes. Among the upregulated genes, one codes for Agaphelin, a 58-amino acid protein containing a single Kazal domain with a Leu in the P1 position. Agaphelin displays high homology to orthologs present in Aedes sp and Culex sp salivary glands, indicating an evolutionarily expanded family. Kinetics and surface plasmon resonance experiments determined that chemically synthesized Agaphelin behaves as a slow and tight inhibitor of neutrophil elastase (K-D similar to 10 nM), but does not affect other enzymes, nor promotes vasodilation, or exhibit antimicrobial activity. TAXIscan chamber assay revealed that Agaphelin inhibits neutrophil chemotaxis toward fMLP, affecting several parameter associated with cell migration. In addition, Agaphelin reduces paw edema formation and accumulation of tissue myeloperoxidase triggered by injection of carrageenan in mice. Agaphelin also blocks elastase/cathepsin-mediated platelet aggregation, abrogates elastase-mediated cleavage of tissue factor pathway inhibitor, and attenuates neutrophil-induced coagulation. Notably, Agaphelin inhibits neutrophil extracellular traps (NETs) formation and prevents FeCl3-induced arterial thrombosis, without impairing hemostasis. Background: Invasion of mosquito salivary glands (SGs) by Plasmodium falciparum sporozoites is an essential step in the malaria life cycle. How infection modulates gene expression, and affects hematophagy remains unclear. Principal Findings: Using Affimetrix chip microarray, we found that at least 43 genes are differentially expressed in the glands of Plasmodium falciparum-infected Anopheles gambiae mosquitoes. Among the upregulated genes, one codes for Agaphelin, a 58-amino acid protein containing a single Kazal domain with a Leu in the P1 position. Agaphelin displays high homology to orthologs present in Aedes sp and Culex sp salivary glands, indicating an evolutionarily expanded family. Kinetics and surface plasmon resonance experiments determined that chemically synthesized Agaphelin behaves as a slow and tight inhibitor of neutrophil elastase (K-D similar to 10 nM), but does not affect other enzymes, nor promotes vasodilation, or exhibit antimicrobial activity. TAXIscan chamber assay revealed that Agaphelin inhibits neutrophil chemotaxis toward fMLP, affecting several parameter associated with cell migration. In addition, Agaphelin reduces paw edema formation and accumulation of tissue myeloperoxidase triggered by injection of carrageenan in mice. Agaphelin also blocks elastase/cathepsin-mediated platelet aggregation, abrogates elastase-mediated cleavage of tissue factor pathway inhibitor, and attenuates neutrophil-induced coagulation. Notably, Agaphelin inhibits neutrophil extracellular traps (NETs) formation and prevents FeCl3-induced arterial thrombosis, without impairing hemostasis.
dcterms:title
Plasmodium falciparum Infection Induces Expression of a Mosquito Salivary Protein (Agaphelin) That Targets Neutrophil Function and Inhibits Thrombosis without Impairing Hemostasis Plasmodium falciparum Infection Induces Expression of a Mosquito Salivary Protein (Agaphelin) That Targets Neutrophil Function and Inhibits Thrombosis without Impairing Hemostasis
skos:prefLabel
Plasmodium falciparum Infection Induces Expression of a Mosquito Salivary Protein (Agaphelin) That Targets Neutrophil Function and Inhibits Thrombosis without Impairing Hemostasis Plasmodium falciparum Infection Induces Expression of a Mosquito Salivary Protein (Agaphelin) That Targets Neutrophil Function and Inhibits Thrombosis without Impairing Hemostasis
skos:notation
RIV/60077344:_____/14:00435190!RIV15-GA0-60077344
n3:aktivita
n8:P n8:I
n3:aktivity
I, P(GAP502/12/2409)
n3:cisloPeriodika
9
n3:dodaniDat
n13:2015
n3:domaciTvurceVysledku
Kotsyfakis, Michalis
n3:druhVysledku
n17:J
n3:duvernostUdaju
n10:S
n3:entitaPredkladatele
n11:predkladatel
n3:idSjednocenehoVysledku
36810
n3:idVysledku
RIV/60077344:_____/14:00435190
n3:jazykVysledku
n16:eng
n3:klicovaSlova
factor pathway inhibitor; platelet aggregation; in vivo; serine proteases; arterial thrombosis; gene expression; structure prediction
n3:klicoveSlovo
n4:gene%20expression n4:serine%20proteases n4:structure%20prediction n4:platelet%20aggregation n4:arterial%20thrombosis n4:factor%20pathway%20inhibitor n4:in%20vivo
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[B8F0CD92FC37]
n3:nazevZdroje
Plos Pathogens
n3:obor
n12:EB
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
18
n3:projekt
n14:GAP502%2F12%2F2409
n3:rokUplatneniVysledku
n13:2014
n3:svazekPeriodika
10
n3:tvurceVysledku
Kotsyfakis, Michalis Leal, A. C. Gera, N. Waisberg, M. Barillas-Mury, C. Gomes, T. Pierce, S. K. Mizurini, D. M. Oliveira, C. J. Monteiro, R.Q. Lukszo, J. Francischetti, I.M.B. Ma, D. Porcella, S. F. Ribeiro, J.M.C. Sousa, B. C. Molina-Cruz, A. Reiter, K.
n3:wos
000343014600010
s:issn
1553-7374
s:numberOfPages
17
n7:doi
10.1371/journal.ppat.1004338