Evidence map›Paper›PMID 26842013›Full record

ArticleCNS neuroscience & therapeutics2016

Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia.

Xin Chen, Fei-Ji Sun, Yu-Jia Wei, Lu-Kang Wang, Zhen-Le Zang, Bing Chen, Song Li, Shi-Yong Liu, Hui Yang

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 20% of its field
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. 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

9 authors at 1 institution in 1 country.

Xin ChenDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Fei-Ji SunDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Yu-Jia WeiDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Lu-Kang WangDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Zhen-Le ZangDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Bing ChenDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Song LiDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Shi-Yong LiuDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Hui YangDepartment of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimFocal cortical dysplasia (FCD) represents a well-known cause of medically intractable epilepsy. Studies found that transient receptor potential vanilloid receptor 4 (TRPV4) may participate in the occurrence of seizures. This study investigated the expression patterns of TRPV4 in FCD and the cascade that regulate functional state of TRPV4 in cortical neurons.

methodsThirty-nine surgical specimens from FCD patients and 10 age-matched control samples from autopsies were included in this study. Protein expression and distribution were detected by Western blot, immunohistochemistry, and immunofluorescence staining. Calcium imaging was used to detect the TRPV4-mediated Ca(2+) influx in cortical neurons.

results(1) The protein levels of TRPV4 and of an upstream factor, protein kinase C (PKC), were markedly elevated in FCD. (2) TRPV4 staining was stronger in the dysplastic cortices of FCD and mainly observed in neuronal microcolumns and malformed cells. (3) The activation of TRPV4 was central for [Ca(2+)]i elevation in cortical neurons, and this activity of TRPV4 in cortical neurons was regulated by the PKC, but not the PKA, pathway.

conclusionThe overexpression and altered cellular distribution of TRPV4 in FCD suggest that TRPV4 may potentially contribute to the epileptogenesis of FCD.

Indexed as

AdolescentAdultAnimalsCalciumChildChild, PreschoolCyclic AMP-Dependent Protein KinasesEpilepsyFemaleHumansInfantMaleMalformations of Cortical DevelopmentNeuronsProtein Kinase CRats, Sprague-DawleyCalciumCyclic AMP-Dependent Protein KinasesProtein Kinase CTRPV4 protein, humanTrpv4 protein, ratTRPV Cation ChannelsCalcium imagingFocal cortical dysplasiaProtein kinase CTRPV4

Identifiers

PMID26842013
PMCPMC6492806
OpenAlexW2284005525

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.