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Arginase 1: An Unexpected Mediator of Pulmonary Capillary Barrier Dysfunction in Models of Acute Lung Injury

Overview of attention for article published in Frontiers in immunology, January 2013
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Title
Arginase 1: An Unexpected Mediator of Pulmonary Capillary Barrier Dysfunction in Models of Acute Lung Injury
Published in
Frontiers in immunology, January 2013
DOI 10.3389/fimmu.2013.00228
Pubmed ID
Authors

Rudolf Lucas, Istvàn Czikora, Supriya Sridhar, Evgeny A. Zemskov, Aluya Oseghale, Sebastian Circo, Stephen D. Cederbaum, Trinad Chakraborty, David J. Fulton, Robert W. Caldwell, Maritza J. Romero

Abstract

The integrity of epithelial and endothelial barriers in the lower airspaces of the lungs has to be tightly regulated, in order to prevent leakage and to assure efficient gas exchange between the alveoli and capillaries. Both G(-) and G(+) bacterial toxins, such as lipopolysaccharide and pneumolysin, respectively, can be released in high concentrations within the pulmonary compartments upon antibiotic treatment of patients suffering from acute respiratory distress syndrome (ARDS) or severe pneumonia. These toxins are able to impair endothelial barrier function, either directly, or indirectly, by induction of pro-inflammatory mediators and neutrophil sequestration. Toxin-induced endothelial hyperpermeability can involve myosin light chain phosphorylation and/or microtubule rearrangement. Endothelial nitric oxide synthase (eNOS) was proposed to be a guardian of basal barrier function, since eNOS knock-out mice display an impaired expression of inter-endothelial junction proteins and as such an increased vascular permeability, as compared to wild type mice. The enzyme arginase, the activity of which can be regulated by the redox status of the cell, exists in two isoforms - arginase 1 (cytosolic) and arginase 2 (mitochondrial) - both of which can be expressed in lung microvascular endothelial cells. Upon activation, arginase competes with eNOS for the substrate l-arginine, as such impairing eNOS-dependent NO generation and promoting reactive oxygen species generation by the enzyme. This mini-review will discuss recent findings regarding the interaction between bacterial toxins and arginase during acute lung injury and will as such address the role of arginase in bacterial toxin-induced pulmonary endothelial barrier dysfunction.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 30%
Student > Master 4 15%
Professor 2 7%
Researcher 2 7%
Student > Doctoral Student 2 7%
Other 4 15%
Unknown 5 19%
Readers by discipline Count As %
Agricultural and Biological Sciences 6 22%
Medicine and Dentistry 5 19%
Biochemistry, Genetics and Molecular Biology 4 15%
Immunology and Microbiology 3 11%
Business, Management and Accounting 1 4%
Other 3 11%
Unknown 5 19%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 September 2013.
All research outputs
#19,944,091
of 25,373,627 outputs
Outputs from Frontiers in immunology
#22,570
of 31,516 outputs
Outputs of similar age
#221,304
of 288,991 outputs
Outputs of similar age from Frontiers in immunology
#240
of 503 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 31,516 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 288,991 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 503 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.