Evidence map›Paper›PMID 23585565›Full record

ArticleThe Journal of biological chemistry2013

Mechanisms of neuroprotection from hypoxia-ischemia (HI) brain injury by up-regulation of cytoglobin (CYGB) in a neonatal rat model.

Shu-Feng Tian, Han-Hua Yang, Dan-Ping Xiao, Yue-Jun Huang, Gu-Yu He, Hai-Ran Ma, Fang Xia, Xue-Chuan Shi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  9. Review
  10. Protective Role of Astrocyte-Derived ExosomalNeuropsychiatric disease and treatment · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cytoglobin at the Crossroads of Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2017
    Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Shu-Feng TianDepartment of Pediatrics, the Second Affiliated Hospital, Shantou University Medical College, North Section of Dong-xia Road, Shantou, Guangdong 515041, China.
Han-Hua Yang
Dan-Ping Xiao
Yue-Jun Huang
Gu-Yu He
Hai-Ran Ma
Fang Xia
Xue-Chuan Shi
Shantou University · CNSecond Affiliated Hospital of Shantou University Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was designed to investigate the expression profile of CYGB, its potential neuroprotective function, and underlying molecular mechanisms using a model of neonatal hypoxia-ischemia (HI) brain injury. Cygb mRNA and protein expression were evaluated within the first 36 h after the HI model was induced using RT-PCR and Western blotting. Cygb mRNA expression was increased at 18 h in a time-dependent manner, and its level of protein expression increased progressively in 24 h. To verify the neuroprotective effect of CYGB, a gene transfection technique was employed. Cygb cDNA and shRNA delivery adenovirus systems were established (Cygb-cDNA-ADV and Cygb-shRNA-ADV, respectively) and injected into the brains of 3-day-old rats 4 days before they were induced with HI treatment. Rats from different groups were euthanized 24 h post-HI, and brain samples were harvested. 2,3,5-Triphenyltetrazolium chloride, TUNEL, and Nissl staining indicated that an up-regulation of CYGB resulted in reduced acute brain injury. The superoxide dismutase level was found to be dependent on expression of CYGB. The Morris water maze test in 28-day-old rats demonstrated that CYGB expression was associated with improvement of long term cognitive impairment. Studies also demonstrated that CYGB can up-regulate mRNA and protein levels of VEGF and increase both the density and diameter of the microvessels but inhibits activation of caspase-2 and -3. Thus, this is the first in vivo study focusing on the neuroprotective role of CYGB. The reduction of neonatal HI injury by CYGB may be due in part to antioxidant and antiapoptotic mechanisms and by promoting angiogenesis.

Indexed as

Up-RegulationAcute DiseaseAdenoviridaeAnimalsAnimals, NewbornAntioxidantsApoptosisBrain InjuriesBrain IschemiaCaspase 3Cerebrovascular CirculationCysteine EndopeptidasesCytoglobinFemaleGlobinsMaleAntioxidantsCasp2 protein, ratCasp3 protein, ratCaspase 3Cygb protein, ratCysteine EndopeptidasesCytoglobinGlobinsNerve Tissue ProteinsRNA, MessengerVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratAngiogenesisApoptosisCytoglobinHypoxiaIschemiaMechanismsNeuroprotection

Identifiers

PMID23585565
PMCPMC3668754
OpenAlexW2003559282

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.