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Salutary effects of glibenclamide during the chronic phase of murine experimental autoimmune encephalomyelitis

Overview of attention for article published in Journal of Neuroinflammation, September 2017
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Title
Salutary effects of glibenclamide during the chronic phase of murine experimental autoimmune encephalomyelitis
Published in
Journal of Neuroinflammation, September 2017
DOI 10.1186/s12974-017-0953-z
Pubmed ID
Authors

Volodymyr Gerzanich, Tapas K. Makar, Poornachander Reddy Guda, Min Seong Kwon, Jesse A. Stokum, Seung Kyoon Woo, Svetlana Ivanova, Alexander Ivanov, Rupal I. Mehta, Alexandra Brooke Morris, Joseph Bryan, Christopher T. Bever, J. Marc Simard

Abstract

In multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), inflammation is perpetuated by both infiltrating leukocytes and astrocytes. Recent work implicated SUR1-TRPM4 channels, expressed mostly by astrocytes, in murine EAE. We tested the hypothesis that pharmacological inhibition of SUR1 during the chronic phase of EAE would be beneficial. EAE was induced in mice using myelin oligodendrocyte glycoprotein (MOG) 35-55. Glibenclamide (10 μg/day) was administered beginning 12 or 24 days later. The effects of treatment were determined by clinical scoring and tissue examination. Drug within EAE lesions was identified using bodipy-glibenclamide. The role of SUR1-TRPM4 in primary astrocytes was characterized using patch clamp and qPCR. Demyelinating lesions from MS patients were studied by immunolabeling and immunoFRET. Administering glibenclamide beginning 24 days after MOG35-55 immunization, well after clinical symptoms had plateaued, improved clinical scores, reduced myelin loss, inflammation (CD45, CD20, CD3, p65), and reactive astrocytosis, improved macrophage phenotype (CD163), and decreased expression of tumor necrosis factor (TNF), B-cell activating factor (BAFF), chemokine (C-C motif) ligand 2 (CCL2) and nitric oxide synthase 2 (NOS2) in lumbar spinal cord white matter. Glibenclamide accumulated within EAE lesions, and had no effect on leukocyte sequestration. In primary astrocyte cultures, activation by TNF plus IFNγ induced de novo expression of SUR1-TRPM4 channels and upregulated Tnf, Baff, Ccl2, and Nos2 mRNA, with glibenclamide blockade of SUR1-TRPM4 reducing these mRNA increases. In demyelinating lesions from MS patients, astrocytes co-expressed SUR1-TRPM4 and BAFF, CCL2, and NOS2. SUR1-TRPM4 may be a druggable target for disease modification in MS.

Twitter Demographics

The data shown below were collected from the profiles of 2 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 35 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 35 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 20%
Student > Master 4 11%
Other 3 9%
Student > Doctoral Student 3 9%
Student > Bachelor 3 9%
Other 7 20%
Unknown 8 23%
Readers by discipline Count As %
Neuroscience 8 23%
Medicine and Dentistry 6 17%
Biochemistry, Genetics and Molecular Biology 5 14%
Nursing and Health Professions 2 6%
Agricultural and Biological Sciences 2 6%
Other 4 11%
Unknown 8 23%

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 31 October 2017.
All research outputs
#8,038,745
of 13,345,024 outputs
Outputs from Journal of Neuroinflammation
#783
of 1,560 outputs
Outputs of similar age
#142,063
of 266,286 outputs
Outputs of similar age from Journal of Neuroinflammation
#8
of 15 outputs
Altmetric has tracked 13,345,024 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,560 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.0. This one is in the 44th percentile – i.e., 44% 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 266,286 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 15 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.