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Pathophysiological significance of the two-pore domain K+ channel K2P5.1 in splenic CD4+CD25− T cell subset from a chemically-induced murine inflammatory bowel disease model

Overview of attention for article published in Frontiers in Physiology, October 2015
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Title
Pathophysiological significance of the two-pore domain K+ channel K2P5.1 in splenic CD4+CD25− T cell subset from a chemically-induced murine inflammatory bowel disease model
Published in
Frontiers in Physiology, October 2015
DOI 10.3389/fphys.2015.00299
Pubmed ID
Authors

Sawa Nakakura, Miki Matsui, Aya Sato, Mizuki Ishii, Kyoko Endo, Sayaka Muragishi, Miki Murase, Hiroaki Kito, Hiroki Niguma, Natsumi Kurokawa, Masanori Fujii, Masatake Araki, Kimi Araki, Susumu Ohya

Abstract

The alkaline pH-activated, two-pore domain K(+) channel K2P5.1 (also known as TASK2/KCNK5) plays an important role in maintaining the resting membrane potential, and contributes to the control of Ca(2+) signaling in several types of cells. Recent studies highlighted the potential role of the K2P5.1 K(+) channel in the pathogenesis of autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. The aim of the present study was to elucidate the pathological significance of the K2P5.1 K(+) channel in inflammatory bowel disease (IBD). The degrees of colitis, colonic epithelial damage, and colonic inflammation were quantified in the dextran sulfate sodium-induced mouse IBD model by macroscopic and histological scoring systems. The expression and functional activity of K2P5.1 in splenic CD4(+) T cells were measured using real-time PCR, Western blot, and fluorescence imaging assays. A significant increase was observed in the expression of K2P5.1 in the splenic CD4(+) T cells of the IBD model. Concomitant with this increase, the hyperpolarization response induced by extracellular alkaline pH was significantly larger in the IBD model with the corresponding intracellular Ca(2+) rises. The expression of K2P5.1 was higher in CD4(+)CD25(-) T cells than in CD4(+)CD25(+) regulatory T cells. The knockout of K2P5.1 in mice significantly suppressed the disease responses implicated in the IBD model. Alternations in intracellular Ca(2+) signaling following the dysregulated expression of K2P5.1 were associated with the disease pathogenesis of IBD. The results of the present study suggest that the K2P5.1 K(+) channel in CD4(+)CD25(-) T cell subset is a potential therapeutic target and biomarker for IBD.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 16 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 16 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 38%
Professor > Associate Professor 2 13%
Lecturer 1 6%
Student > Doctoral Student 1 6%
Professor 1 6%
Other 3 19%
Unknown 2 13%
Readers by discipline Count As %
Immunology and Microbiology 3 19%
Neuroscience 3 19%
Agricultural and Biological Sciences 3 19%
Pharmacology, Toxicology and Pharmaceutical Science 2 13%
Medicine and Dentistry 2 13%
Other 1 6%
Unknown 2 13%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 19 November 2015.
All research outputs
#16,599,928
of 26,184,649 outputs
Outputs from Frontiers in Physiology
#6,163
of 15,778 outputs
Outputs of similar age
#159,765
of 296,580 outputs
Outputs of similar age from Frontiers in Physiology
#53
of 113 outputs
Altmetric has tracked 26,184,649 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 15,778 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one has gotten more attention than average, scoring higher than 58% of its peers.
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 296,580 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 113 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 51% of its contemporaries.