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Experimental acute lung injury induces multi-organ epigenetic modifications in key angiogenic genes implicated in sepsis-associated endothelial dysfunction

Overview of attention for article published in Critical Care, December 2015
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About this Attention Score

  • Good Attention Score compared to outputs of the same age (70th percentile)

Mentioned by

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9 tweeters

Citations

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34 Dimensions

Readers on

mendeley
73 Mendeley
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Title
Experimental acute lung injury induces multi-organ epigenetic modifications in key angiogenic genes implicated in sepsis-associated endothelial dysfunction
Published in
Critical Care, December 2015
DOI 10.1186/s13054-015-0943-4
Pubmed ID
Authors

Karol Bomsztyk, Daniel Mar, Dowon An, Roya Sharifian, Michal Mikula, Sina A Gharib, William A Altemeier, W Conrad Liles, Oleg Denisenko

Abstract

The Tie-2/angiopoietin (Tie-2/Ang) and vascular endothelial growth factor receptor-ligand systems (VEGFR/VEGF) are recognized to play important roles in the regulation of microvascular endothelial function. Downregulation of these genes during sepsis has been implicated in the pathogenesis of sepsis-related microvascular leak and multiple organ dysfunction syndrome (MODS). Mechanisms responsible for dysregulation of angiogenic genes in sepsis are poorly defined. Western blot, RT PCR and multiplex chromatin immunoprecipitation platform (Matrix ChIP) were used to investigate serum albumin leak, changes in gene expression and associated epigenetic alterations in a murine model of acute lung injury-induced sepsis (ALI-sepsis). Experimental ALI-sepsis induced microvascular leak and downregulation of expression of Angpt1 (Ang1), Tek (Tie-2) and Kdr (Vegfr2 or Flk-1) genes in lung, kidney and liver. These changes correlate with a decrease in RNA polymerase II (Pol II) density at these genes, with the greatest response observed in the lung. ALI-sepsis reduced levels of transcription-permissive histone H3 lysine acetylation (H3KAc) at these loci in all examined tissues. Decreases in permissive H3K4m3 and H3Km2 marks were detected only in lung. In contrast, only minimal alterations in transcription-repressive histone modifications (H3K27m3, H3K9m2, H3K9m3 and H4K20m3) were observed in all tissues. Our results demonstrate that decreases in transcription-permissive, but not increases in transcription-repressive, histone modifications at Angpt1, Tek and Kdr is a systemic, rather than a lung-restricted response, involving key end-organs in experimental ALI-sepsis. Given that ventilator-associated pneumonia is a major cause of sepsis in critically ill patients, elucidation of mechanisms mediating epigenetic alterations during sepsis provides fundamental new insights into the pathogenesis of sepsis-induced microvascular leak and subsequent end-organ injury/dysfunction.

Twitter Demographics

The data shown below were collected from the profiles of 9 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 73 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 1%
Belgium 1 1%
Brazil 1 1%
Unknown 70 96%

Demographic breakdown

Readers by professional status Count As %
Student > Master 16 22%
Student > Ph. D. Student 12 16%
Researcher 9 12%
Professor > Associate Professor 6 8%
Professor 4 5%
Other 13 18%
Unknown 13 18%
Readers by discipline Count As %
Medicine and Dentistry 29 40%
Biochemistry, Genetics and Molecular Biology 12 16%
Agricultural and Biological Sciences 11 15%
Immunology and Microbiology 2 3%
Nursing and Health Professions 1 1%
Other 5 7%
Unknown 13 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 4. 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 11 June 2015.
All research outputs
#5,682,032
of 19,214,062 outputs
Outputs from Critical Care
#3,278
of 5,568 outputs
Outputs of similar age
#70,821
of 240,809 outputs
Outputs of similar age from Critical Care
#2
of 4 outputs
Altmetric has tracked 19,214,062 research outputs across all sources so far. This one has received more attention than most of these and is in the 70th percentile.
So far Altmetric has tracked 5,568 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 17.4. This one is in the 40th percentile – i.e., 40% 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 240,809 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 70% of its contemporaries.
We're also able to compare this research output to 4 others from the same source and published within six weeks on either side of this one. This one has scored higher than 2 of them.