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The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

Overview of attention for article published in Journal of Neuroinflammation, October 2017
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Title
The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke
Published in
Journal of Neuroinflammation, October 2017
DOI 10.1186/s12974-017-0973-8
Pubmed ID
Authors

Mengni Yi, Tianjiao Wei, Yanxia Wang, Qin Lu, Gaoxian Chen, Xiaoling Gao, Herbert M. Geller, Hongzhuan Chen, Zhihua Yu

Abstract

Reactive astrogliosis is one of the significantly pathological features in ischemic stroke accompanied with changes in gene expression, morphology, and proliferation. KCa3.1 was involved in TGF-β-induced astrogliosis in vitro and also contributed to astrogliosis-mediated neuroinflammation in neurodegeneration disease. Wild type mice and KCa3.1(-/-) mice were subjected to permanent middle cerebral artery occlusion (pMCAO) to evaluate the infarct areas by 2,3,5-triphenyltetrazolium hydrochloride staining and neurological deficit. KCa3.1 channels expression and cell localization in the brain of pMCAO mice model were measured by immunoblotting and immunostaining. Glia activation and neuron loss was measured by immunostaining. DiBAC4 (3) and Fluo-4AM were used to measure membrane potential and cytosolic Ca(2+) level in oxygen-glucose deprivation induced reactive astrocytes in vitro. Immunohistochemistry on pMCAO mice infarcts showed strong upregulation of KCa3.1 immunoreactivity in reactive astrogliosis. KCa3.1(-/-) mice exhibited significantly smaller infarct areas on pMCAO and improved neurological deficit. Both activated gliosis and neuronal loss were attenuated in KCa3.1(-/-) pMCAO mice. In the primary cultured astrocytes, the expressions of KCa3.1 and TRPV4 were increased associated with upregulation of astrogliosis marker GFAP induced by oxygen-glucose deprivation. The activation of KCa3.1 hyperpolarized membrane potential and, by promoting the driving force for calcium, induced calcium entry through TRPV4, a cation channel of the transient receptor potential family. Double-labeled staining showed that KCa3.1 and TRPV4 channels co-localized in astrocytes. Blockade of KCa3.1 or TRPV4 inhibited the phenotype switch of reactive astrogliosis. Our data suggested that KCa3.1 inhibition might represent a promising therapeutic strategy for ischemia stroke.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 25 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 20%
Student > Master 4 16%
Researcher 3 12%
Student > Bachelor 2 8%
Other 1 4%
Other 1 4%
Unknown 9 36%
Readers by discipline Count As %
Neuroscience 6 24%
Medicine and Dentistry 3 12%
Agricultural and Biological Sciences 2 8%
Biochemistry, Genetics and Molecular Biology 2 8%
Nursing and Health Professions 1 4%
Other 1 4%
Unknown 10 40%
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 19 October 2017.
All research outputs
#20,450,513
of 23,006,268 outputs
Outputs from Journal of Neuroinflammation
#2,323
of 2,653 outputs
Outputs of similar age
#284,211
of 325,925 outputs
Outputs of similar age from Journal of Neuroinflammation
#33
of 43 outputs
Altmetric has tracked 23,006,268 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,653 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 43 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.