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Article ; Online: Schistosomiasis-associated pulmonary hypertension unveils disrupted murine gut-lung microbiome and reduced endoprotective Caveolin-1/BMPR2 expression.

Marinho, Ygor / Villarreal, Elizabeth S / Aboagye, Sammy Y / Williams, David L / Sun, Jun / Silva, Claudia L M / Lutz, Sarah E / Oliveira, Suellen D

Frontiers in immunology

2023 Volume 14, Page(s) 1254762

Abstract: Schistosomiasis-associated Pulmonary Arterial Hypertension (Sch-PAH) is a life-threatening complication of ... ...

Abstract	Schistosomiasis-associated Pulmonary Arterial Hypertension (Sch-PAH) is a life-threatening complication of chronic
MeSH term(s)	Animals ; Mice ; Bone Morphogenetic Protein Receptors, Type II/genetics ; Bone Morphogenetic Protein Receptors, Type II/metabolism ; Caveolin 1/genetics ; Endothelial Cells/metabolism ; Gastrointestinal Microbiome ; Hypertension, Pulmonary/etiology ; Lung/pathology ; Pulmonary Arterial Hypertension/etiology ; Pulmonary Arterial Hypertension/pathology ; Pulmonary Artery/metabolism ; Pulmonary Artery/pathology ; Schistosomiasis/metabolism
Chemical Substances	Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30) ; Caveolin 1 ; Bmpr2 protein, mouse (EC 2.7.11.30) ; Cav1 protein, mouse
Language	English
Publishing date	2023-10-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1254762
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Caveolin and Endothelial NO Signaling.

Oliveira, Suellen D S / Minshall, Richard D

Current topics in membranes

2018 Volume 82, Page(s) 257–279

Abstract: Pulmonary vascular diseases are associated with several factors including infection, cigarette smoking, abuse of dietary suppressants and drugs, prolonged exposure to high altitude, and other causes which in part induce significant oxidative stress ... ...

Abstract	Pulmonary vascular diseases are associated with several factors including infection, cigarette smoking, abuse of dietary suppressants and drugs, prolonged exposure to high altitude, and other causes which in part induce significant oxidative stress resulting in endothelial cell injury, apoptosis, hyperproliferation, and vaso-occlusive disease. Maintenance of normal endothelial cell function is a critical role of endothelial nitric oxide synthase (eNOS) activity and physiologic nitric oxide (NO) signaling in the vascular wall. eNOS expression and activity is regulated by the membrane-associated scaffolding protein caveolin-1 (Cav-1), the main protein constituent of caveolae. This chapter summarizes the literature and highlights unanswered questions related to how inflammation-associated oxidative stress affects Cav-1 expression and regulatory functions, and how dysregulated eNOS enzymatic activity promotes endothelial dysfunction. Focus is given to how the conversion of eNOS from a NO-producing enzyme to a transient oxidant-generating system is associated twith Cav-1 depletion, endothelial cell injury, and pulmonary vascular diseases. Importantly, the vascular defects observed in absence of Cav-1 that give rise to injured or hyperproliferative endothelial cells and promote remodeled vasculature can be rescued by "re-coupling," inhibiting, or genetically deleting eNOS, supporting the notion that strict control of Cav-1 expression and eNOS activity and signaling is critical for maintaining pulmonary vascular homeostasis.
MeSH term(s)	Caveolin 1/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Humans ; Lung/cytology ; Lung/metabolism ; Mechanotransduction, Cellular ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Signal Transduction
Chemical Substances	Caveolin 1 ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2018-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1063-5823
ISSN	1063-5823
DOI	10.1016/bs.ctm.2018.09.004
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Article ; Online: Targeting chalcone binding sites in living Leishmania using a reversible fluorogenic benzochalcone probe.

Batista, Ariane S / Oliveira, Suellen D S / Pomel, Sébastien / Commere, Pierre-Henri / Mazan, Valérie / Lee, Moses / Loiseau, Philippe M / Rossi-Bergmann, Bartira / Prina, Eric / Duval, Romain

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2022 Volume 149, Page(s) 112784

Abstract: Chalcones (1,3-diphenyl-2-propen-1-ones) either natural or synthetic have a plethora of biological properties including antileishmanial activities, but their development as drugs is hampered by their largely unknown mechanisms of action. We demonstrate ... ...

Abstract	Chalcones (1,3-diphenyl-2-propen-1-ones) either natural or synthetic have a plethora of biological properties including antileishmanial activities, but their development as drugs is hampered by their largely unknown mechanisms of action. We demonstrate herein that our previously described benzochalcone fluorogenic probe (HAB) could be imaged by fluorescence microscopy in live Leishmania amazonensis promastigotes where it targeted the parasite acidocalcisomes, lysosomes and the mitochondrion. As in the live zebrafish model, HAB formed yellow-emitting fluorescent complexes when associated with biological targets in Leishmania. Further, we used HAB as a reversible probe to study the binding of a portfolio of diverse chalcones and analogues in live promastigotes, using a combination of competitive flow cytometry analysis and cell microscopy. This pharmacological evaluation suggested that the binding of HAB in promastigotes was representative of chalcone pharmacology in Leishmania, with certain exogenous chalcones exhibiting competitive inhibition (ca. 20-30%) towards HAB whereas non-chalconic inhibitors showed weak capacity (ca. 3-5%) to block the probe intracellular binding. However, this methodology was restricted by the strong toxicity of several competing chalcones at high concentration, in conjunction with the limited sensitivity of the HAB fluorophore. This advocates for further optimization of this undirect target detection strategy using pharmacophore-derived reversible fluorescent probes.
MeSH term(s)	Animals ; Antiprotozoal Agents/chemistry ; Antiprotozoal Agents/pharmacology ; Binding Sites ; Chalcone/pharmacology ; Chalcones/chemistry ; Chalcones/pharmacology ; Fluorescent Dyes ; Leishmania ; Zebrafish
Chemical Substances	Antiprotozoal Agents ; Chalcones ; Fluorescent Dyes ; Chalcone (5S5A2Q39HX)
Language	English
Publishing date	2022-03-14
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2022.112784
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Article: Ultraspecific live imaging of the dynamics of zebrafish neutrophil granules by a histopermeable fluorogenic benzochalcone probe.

Colucci-Guyon, Emma / Batista, Ariane S / Oliveira, Suellen D S / Blaud, Magali / Bellettini, Ismael C / Marteyn, Benoit S / Leblanc, Karine / Herbomel, Philippe / Duval, Romain

Chemical science

2019 Volume 10, Issue 12, Page(s) 3654–3670

Abstract: Neutrophil granules (NGs) are key components of the innate immune response and mark the development of neutrophilic granulocytes in mammals. However, there has been no specific fluorescent vital stain up to now to monitor their dynamics within a whole ... ...

Abstract	Neutrophil granules (NGs) are key components of the innate immune response and mark the development of neutrophilic granulocytes in mammals. However, there has been no specific fluorescent vital stain up to now to monitor their dynamics within a whole live organism. We rationally designed a benzochalcone fluorescent probe (
Language	English
Publishing date	2019-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2559110-1
ISSN	2041-6539 ; 2041-6520
ISSN (online)	2041-6539
ISSN	2041-6520
DOI	10.1039/c8sc05593a
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Article: Blood plasma proteome alteration after local tissue damage induced by Bothrops erythromelas snake venom in mice

Cavalcante, Joeliton S. / da Silva, Weslley G. / de Oliveira, Laudicéia Alves / Brito, Ingrid Mayara C. / Muller, Kevin S. / Vidal, Ivynna Suellen / dos Santos, Lucilene D. / Jorge, Roberta Jeane Bezerra / Almeida, Cayo / de Lima Bicho, Carla

Journal of proteomics. 2022 Sept. 22,

2022

Abstract: Snakes of the genus Bothrops are responsible the most snakebites in the Brazil, causing a diverse and complex pathophysiological condition. Bothrops erythromelas is the main specie of medical relevance found in the Caatinga from the Brazilian Northeast ... ...

Abstract	Snakes of the genus Bothrops are responsible the most snakebites in the Brazil, causing a diverse and complex pathophysiological condition. Bothrops erythromelas is the main specie of medical relevance found in the Caatinga from the Brazilian Northeast region. The pathophysiological effects involving B. erythromelas snakebite as well as the organism reaction in response to this envenomation are not so explored. Thus, edema was induced in mice paws using 2.5 μg or 5.0 μg of B. erythromelas venom, and the percentage of edema was measured. Plasma was collected 30 min after the envenomation-induced in mice and analyzed by mass spectrometry. It was identified a total of 112 common plasma proteins differentially abundant among experimental groups, which are involved with the complement system and coagulation cascades, oxidative stress, neutrophil degranulation, platelets degranulation and inflammatory response. Apolipoprotein A1 (Apoa), serum amyloid protein A-4 (Saa4), adiponectin (Adipoq) showed up-regulated in mice plasma after injection of venom, while fibulin (Fbln1), factor XII (F12) and vitamin K-dependent protein Z (Proz) showed down-regulated. The results indicate a protein pattern of thrombo-inflammation to the B. erythromelas snakebite, evidencing potential biomarkers for monitoring this snakebite, new therapeutic targets and its correlations with the degree of envenomation once showed modulations in the abundance among the different groups according to the amount of venom injected into the mice.
Keywords	Bothrops ; adiponectin ; amyloid ; apolipoprotein A-I ; biomarkers ; blood serum ; caatinga ; coagulation ; complement ; edema ; inflammation ; mass spectrometry ; neutrophils ; oxidative stress ; proteome ; proteomics ; snake bites ; snake venoms ; therapeutics ; Brazil
Language	English
Dates of publication	2022-0922
Publishing place	Elsevier B.V.
Document type	Article
Note	Pre-press version
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2022.104742
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: S. mansoni SmKI-1 Kunitz-domain: Leucine point mutation at P1 site generates enhanced neutrophil elastase inhibitory activity.

Mambelli, Fábio / Santos, Bruno P O / Morais, Suellen B / Gimenez, Enrico G T / Astoni, Duana C Dos S / Braga, Amanda D / Ferreira, Rafaela S / Amaral, Flávio A / de Magalhães, Mariana T Q / Oliveira, Sergio C

PLoS neglected tropical diseases

2021 Volume 15, Issue 1, Page(s) e0009007

Abstract: ... given its central role for KD's inhibition to NE. We have also substituted a glutamic acid that strongly interacts ...

Abstract	The Schistosoma mansoni SmKI-1 protein is composed of two domains: a Kunitz-type serine protease inhibitor motif (KD) and a C-terminus domain with no similarity outside the genera. Our previous work has demonstrated that KD plays an essential role in neutrophil elastase (NE) binding blockage, in neutrophil influx and as a potential anti-inflammatory molecule. In order to enhance NE blocking capacity, we analyzed the KD sequence from a structure-function point of view and designed specific point mutations in order to enhance NE affinity. We substituted the P1 site residue at the reactive site for a leucine (termed RL-KD), given its central role for KD's inhibition to NE. We have also substituted a glutamic acid that strongly interacts with the P1 residue for an alanine, to help KD to be buried on NE S1 site (termed EA-KD). KD and the mutant proteins were evaluated in silico by molecular docking to human NE, expressed in Escherichia coli and tested towards its NE inhibitory activity. Both mutated proteins presented enhanced NE inhibitory activity in vitro and RL-KD presented the best performance. We further tested RL-KD in vivo in an experimental model of monosodium urate (MSU)-induced acute arthritis. RL-KD showed reduced numbers of total cells and neutrophils in the mouse knee cavity when compared to KD. Nevertheless, both RL-KD and KD reduced mice hypernociception in a similar fashion. In summary, our results demonstrated that both mutated proteins showed enhanced NE inhibitory activity in vitro. However, RL-KD had a prominent effect in diminishing inflammatory parameters in vivo.
MeSH term(s)	Animals ; Arthritis ; Leucine/chemistry ; Leucine/drug effects ; Leucine/genetics ; Leucine/metabolism ; Leukocyte Elastase/drug effects ; Mice ; Molecular Docking Simulation ; Neutrophils ; Point Mutation ; Proteinase Inhibitory Proteins, Secretory/chemistry ; Proteinase Inhibitory Proteins, Secretory/genetics ; Proteinase Inhibitory Proteins, Secretory/metabolism ; Proteinase Inhibitory Proteins, Secretory/pharmacology ; Recombinant Proteins ; Schistosoma mansoni/genetics ; Schistosoma mansoni/metabolism ; Structure-Activity Relationship ; Substrate Specificity ; Toll-Like Receptor 4/genetics ; Transcriptome
Chemical Substances	Proteinase Inhibitory Proteins, Secretory ; Recombinant Proteins ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Leukocyte Elastase (EC 3.4.21.37) ; Leucine (GMW67QNF9C)
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2727
ISSN (online)	1935-2735
ISSN	1935-2727
DOI	10.1371/journal.pntd.0009007
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: P2X7 receptor activation increases expression of caveolin-1 and formation of macrophage lipid rafts, thereby boosting CD39 activity.

Savio, Luiz Eduardo Baggio / de Andrade Mello, Paola / Santos, Stephanie Alexia Cristina Silva / de Sousa, Júlia Costa / Oliveira, Suellen D S / Minshall, Richard D / Kurtenbach, Eleonora / Wu, Yan / Longhi, Maria Serena / Robson, Simon C / Coutinho-Silva, Robson

Journal of cell science

2020 Volume 133, Issue 5

Abstract: Macrophages are tissue-resident immune cells that are crucial for the initiation and maintenance of immune responses. Purinergic signaling modulates macrophage activity and impacts cellular plasticity. The ATP-activated purinergic receptor P2X7 (also ... ...

Abstract	Macrophages are tissue-resident immune cells that are crucial for the initiation and maintenance of immune responses. Purinergic signaling modulates macrophage activity and impacts cellular plasticity. The ATP-activated purinergic receptor P2X7 (also known as P2RX7) has pro-inflammatory properties, which contribute to macrophage activation. P2X7 receptor signaling is, in turn, modulated by ectonucleotidases, such as CD39 (also known as ENTPD1), expressed in caveolae and lipid rafts. Here, we examined P2X7 receptor activity and determined impacts on ectonucleotidase localization and function in macrophages primed with lipopolysaccharide (LPS). First, we verified that ATP boosts CD39 activity and caveolin-1 protein expression in LPS-primed macrophages. Drugs that disrupt cholesterol-enriched domains - such as nystatin and methyl-β-cyclodextrin - decreased CD39 enzymatic activity in all circumstances. We noted that CD39 colocalized with lipid raft markers (flotillin-2 and caveolin-1) in macrophages that had been primed with LPS followed by treatment with ATP. P2X7 receptor inhibition blocked these ATP-mediated increases in caveolin-1 expression and inhibited the colocalization with CD39. Further, we found that STAT3 activation is significantly attenuated caveolin-1-deficient macrophages treated with LPS or LPS+BzATP. Taken together, our data suggest that P2X7 receptor triggers the initiation of lipid raft-dependent mechanisms that upregulates CD39 activity and could contribute to limit macrophage responses restoring homeostasis.
MeSH term(s)	Adenosine Triphosphate ; Caveolin 1/genetics ; Lipopolysaccharides ; Macrophages ; Membrane Microdomains ; Receptors, Purinergic P2X7/genetics
Chemical Substances	Caveolin 1 ; Lipopolysaccharides ; Receptors, Purinergic P2X7 ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2020-03-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.237560
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Article: Pediatric Acute Promyelocytic Leukemia: Epidemiology, Molecular Features, and Importance of GST-Theta 1 in Chemotherapy Response and Outcome.

Andrade, Francianne G / Feliciano, Suellen V M / Sardou-Cezar, Ingrid / Brisson, Gisele D / Dos Santos-Bueno, Filipe V / Vianna, Danielle T / Marques, Luísa V C / Terra-Granado, Eugênia / Zalcberg, Ilana / Santos, Marceli de O / Costa, Juliana T / Noronha, Elda P / Thuler, Luiz C S / Wiemels, Joseph L / Pombo-de-Oliveira, Maria S

Frontiers in oncology

2021 Volume 11, Page(s) 642744

Abstract: ... deletion in glutathione S-transferases (GSTs) leads to a loss of enzyme detoxification activity, possibly ...

Abstract	Previous studies have suggested a variation in the incidence of acute promyelocytic leukemia (APL) among the geographic regions with relatively higher percentages in the Latin American population. We aimed to explore the population burden of pediatric APL, gathering information from the population-based cancer registry (PBCR) and the diagnosis of APL obtained through incident cases from a hospital-based cohort. The homozygous deletion in glutathione S-transferases (GSTs) leads to a loss of enzyme detoxification activity, possibly affecting the treatment response. Mutations in the
Language	English
Publishing date	2021-03-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.642744
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Article ; Online: S. mansoni SmKI-1 Kunitz-domain

Fábio Mambelli / Bruno P O Santos / Suellen B Morais / Enrico G T Gimenez / Duana C Dos S Astoni / Amanda D Braga / Rafaela S Ferreira / Flávio A Amaral / Mariana T Q de Magalhães / Sergio C Oliveira

PLoS Neglected Tropical Diseases, Vol 15, Iss 1, p e

Leucine point mutation at P1 site generates enhanced neutrophil elastase inhibitory activity.

2021 Volume 0009007

Abstract: ... given its central role for KD's inhibition to NE. We have also substituted a glutamic acid that strongly interacts ...

Abstract	The Schistosoma mansoni SmKI-1 protein is composed of two domains: a Kunitz-type serine protease inhibitor motif (KD) and a C-terminus domain with no similarity outside the genera. Our previous work has demonstrated that KD plays an essential role in neutrophil elastase (NE) binding blockage, in neutrophil influx and as a potential anti-inflammatory molecule. In order to enhance NE blocking capacity, we analyzed the KD sequence from a structure-function point of view and designed specific point mutations in order to enhance NE affinity. We substituted the P1 site residue at the reactive site for a leucine (termed RL-KD), given its central role for KD's inhibition to NE. We have also substituted a glutamic acid that strongly interacts with the P1 residue for an alanine, to help KD to be buried on NE S1 site (termed EA-KD). KD and the mutant proteins were evaluated in silico by molecular docking to human NE, expressed in Escherichia coli and tested towards its NE inhibitory activity. Both mutated proteins presented enhanced NE inhibitory activity in vitro and RL-KD presented the best performance. We further tested RL-KD in vivo in an experimental model of monosodium urate (MSU)-induced acute arthritis. RL-KD showed reduced numbers of total cells and neutrophils in the mouse knee cavity when compared to KD. Nevertheless, both RL-KD and KD reduced mice hypernociception in a similar fashion. In summary, our results demonstrated that both mutated proteins showed enhanced NE inhibitory activity in vitro. However, RL-KD had a prominent effect in diminishing inflammatory parameters in vivo.
Keywords	Arctic medicine. Tropical medicine ; RC955-962 ; Public aspects of medicine ; RA1-1270
Subject code	570
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Injury-Induced Shedding of Extracellular Vesicles Depletes Endothelial Cells of Cav-1 (Caveolin-1) and Enables TGF-β (Transforming Growth Factor-β)-Dependent Pulmonary Arterial Hypertension.

Oliveira, Suellen D S / Chen, Jiwang / Castellon, Maricela / Mao, Mao / Raj, J Usha / Comhair, Suzy / Erzurum, Serpil / Silva, Claudia L M / Machado, Roberto F / Bonini, Marcelo G / Minshall, Richard D

Arteriosclerosis, thrombosis, and vascular biology

2019 Volume 39, Issue 6, Page(s) 1191–1202

Abstract: Objective- To determine whether pulmonary arterial hypertension is associated with endothelial cell (EC)-Cav-1 (caveolin-1) depletion, EC-derived extracellular vesicle cross talk with macrophages, and proliferation of Cav-1 depleted ECs via TGF-β ( ... ...

Abstract	Objective- To determine whether pulmonary arterial hypertension is associated with endothelial cell (EC)-Cav-1 (caveolin-1) depletion, EC-derived extracellular vesicle cross talk with macrophages, and proliferation of Cav-1 depleted ECs via TGF-β (transforming growth factor-β) signaling. Approach and Results- Pulmonary vascular disease was induced in Sprague-Dawley rats by exposure to a single injection of VEGFRII (vascular endothelial growth factor receptor II) antagonist SU5416 (Su) followed by hypoxia (Hx) plus normoxia (4 weeks each-HxSu model) and in WT (wild type; Tie2.Cre
MeSH term(s)	Adolescent ; Adult ; Aged ; Animals ; Bone Morphogenetic Protein Receptors, Type II/metabolism ; Case-Control Studies ; Caveolin 1/deficiency ; Caveolin 1/genetics ; Cell Proliferation ; Disease Models, Animal ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/pathology ; Female ; Humans ; Hypoxia/complications ; Indoles ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Pulmonary Arterial Hypertension/etiology ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Arterial Hypertension/pathology ; Pyrroles ; Rats, Sprague-Dawley ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta/metabolism ; Vascular Remodeling ; Young Adult
Chemical Substances	CAV1 protein, human ; Cav1 protein, mouse ; Cav1 protein, rat ; Caveolin 1 ; Indoles ; Pyrroles ; Smad Proteins ; Transforming Growth Factor beta ; Semaxinib (71IA9S35AJ) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39) ; Bmpr2 protein, mouse (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30)
Language	English
Publishing date	2019-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.118.312038
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