Evidence map›Paper›PMID 27339639›Full record

ArticleJournal of physiology and biochemistry2016

Critical role of regulator of calcineurin 1 in spinal cord injury.

Guodong Wang, Yilei Zhao, Shenpeng Liu, Jinling Jia, Tan Lu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Spatiotemporal expression of RCAN1 and its isoformThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    Article
  3. Article
  4. Review
  5. Calcineurin Dysregulation Underlies Spinal Cord Injury-Induced KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

5 authors at 1 institution in 1 country.

Guodong WangDepartment of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, People's Republic of China. guodong_wang02@163.com.
Yilei ZhaoDepartment of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, People's Republic of China.
Shenpeng LiuDepartment of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, People's Republic of China.
Jinling JiaDepartment of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, People's Republic of China.
Tan LuDepartment of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, People's Republic of China.
First Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal cord injury (SCI) is a severe clinical problem worldwide. The pathogenesis of SCI is complicated and much is unknown. The current study was designed to investigate the possible role of regulator of calcineurin 1 (RCAN1) in SCI and to explore the possible molecular mechanisms. Rats were injected with LVshRNAi-RCAN1 and then contusion-induced SCI was established. We found that RCAN1 was significantly increased in spinal cord of rats with SCI. Knockdown of RCAN1 markedly facilitated the structural and functional recovery in the spinal cord, as illustrated by decrease of lesion volume and increase of Basso, Beattie, and Bresnahan (BBB) and combined behavioral score (CBS) scores. Downregulation of RCAN1 suppressed the increase of pro-inflammatory cytokines, including IL-1β and TNF-α, and inhibited the increase of TUNEL-positive cell numbers and caspases 3 and 9 activities. The decrease of oxygen consumption rate and increase of expression of glucose-regulated protein 78 (GRP78) and phosphorylation of protein kinase RNA-like endoplasmic reticulum (ER) kinase (PERK) in rats with SCI were inhibited by LVshRNAi-RCAN1. Moreover, knockdown of RCAN1 ameliorated oxidative stress in rats with SCI, as evidenced by decrease of TBA reactive substances (TBARS) and GSSG content and increase of glutathione (GSH) level. These results suggested that RCAN1 played an important role in SCI through regulation of various pathological processes. Overall, the data provide novel insights into the role of RCAN1 in SCI and novel therapeutic targets of the treatment of injury in the spinal cord.

Indexed as

Signal TransductionAnimalsCaspase 3Caspase 9eIF-2 KinaseEndoplasmic Reticulum Chaperone BiPGene Expression RegulationGlutathioneHeat-Shock ProteinsInterleukin-1betaIntracellular Signaling Peptides and ProteinsMaleOxidative StressPhosphorylationRatsRats, Sprague-DawleyCasp3 protein, ratCasp9 protein, ratCaspase 3Caspase 9eIF-2 KinaseEndoplasmic Reticulum Chaperone BiPGlutathioneGRP78 protein, ratHeat-Shock ProteinsIL1B protein, ratInterleukin-1betaIntracellular Signaling Peptides and ProteinsRCAN1 protein, ratRNA, Small InterferingThiobarbituric Acid Reactive SubstancesTumor Necrosis Factor-alphaApoptosisInflammationOxidative stressRegulator of calcineurin 1Spinal cord injury

Identifiers

PMID27339639
OpenAlexW2471781813

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.