Evidence map›Paper›PMID 29348796›Full record

ArticleInternational journal of physiology, pathophysiology and pharmacology2017

Condition-specific transcriptional regulation of neuronal ion channel genes in brain ischemia.

Luisa Hernandez-Encarnacion, Pankaj Sharma, Roger Simon, An Zhou

Abstract read
In one paragraph

Article in International journal of physiology, pathophysiology and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Luisa Hernandez-EncarnacionDepartment of Neurobiology, Neuroscience Institute, Morehouse School of MedicineAtlanta, Georgia, USA.
Pankaj SharmaDepartment of Neurobiology, Neuroscience Institute, Morehouse School of MedicineAtlanta, Georgia, USA.
Roger SimonDepartment of Neurobiology, Neuroscience Institute, Morehouse School of MedicineAtlanta, Georgia, USA.
An ZhouDepartment of Neurobiology, Neuroscience Institute, Morehouse School of MedicineAtlanta, Georgia, USA.

Funding

Morehouse School of Medicine Center of Excellence Research Endowment ProgramS21MD000101 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI MONTGOMERY-RICE, VALERIE C. · 2001 to 2015
$74.3M
Program Evaluation - Internal & External U54NS083932 · NINDS · MOREHOUSE SCHOOL OF MEDICINE · PI MACLEISH, PETER RAYMOND · 2013 to 2017
$7.7M
POLYCOMB GROUP PROTEINS AS EPIGENETIC MEDIATORS OF BRAIN ISCHEMIC TOLERANCER01NS073832 · NINDS · MOREHOUSE SCHOOL OF MEDICINE · PI ZHOU, AN · 2012 to 2015
$1.2M
NIMHD NIH HHS S21 MD000101NINDS NIH HHS R01 NS073832NINDS NIH HHS U54 NS083932
6 · The paper itself

Abstract

In the context of seeking novel therapeutic targets for treating ischemic stroke, the preconditioning ischemia-induced brain ischemic tolerance has been used as a model of endogenously operative, broad-based neuroprotective mechanisms. Targeting such mechanisms is considered potentially less prone to adverse side effects, as those seen in many failed clinical trials that focus on single targets using exogenous compounds. Results from previous studies have revealed an overall decrease in potassium channel activity in tolerance development. The objective of this study is to identify ion channel genes that are differentially regulated under different brain ischemic conditions, as a mean to identify those ion channels that are associated with ischemic brain injury and ischemic tolerance. In mice in vivo, transient focal cerebral ischemia was induced by middle cerebral artery occlusion. In cultured neuronal cells in vitro, simulated ischemia was modeled by oxygen-glucose deprivation. For both in vivo and in vitro studies, three principal ischemic conditions were included: ischemic-preconditioned, injured and tolerant, respectively, plus appropriate controls. In these model systems, transcript levels of a panel of 84 neuronal ion channels genes were analyzed with a quantitative real-time PCR mini-array. The results showed that, both in vivo and in vitro, there was a predominant down regulation in neuronal ion channel genes under ischemic-tolerant conditions, and an up regulation in ischemic injury. Similar changes were observed among potassium, sodium and calcium channel genes. A number of regulated genes exhibited opposing changes under ischemic-injured and ischemic-tolerant conditions. This subset of ion channel genes exemplifies potentially novel leads for developing multi-factorial therapeutic targets for treating ischemic stroke.

Indexed as

ion channelsIschemic strokeneuronal excitabilityneuroprotection

Identifiers

PMID29348796
PMCPMC5770516

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.