Evidence map›Paper›PMID 27455253›Full record

ArticleInternational journal of molecular sciences2016

Homocysteine Aggravates Cortical Neural Cell Injury through Neuronal Autophagy Overactivation following Rat Cerebral Ischemia-Reperfusion.

Yaqian Zhao, Guowei Huang, Shuang Chen, Yun Gou, Zhiping Dong, Xumei Zhang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 63 citations in OpenAlex.

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  12. International journal of molecular sciences · 2021
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  16. Irisin: A Promising Target for Ischemia-Reperfusion Injury Therapy.Oxidative medicine and cellular longevity · 2021
    Review
  17. Article
  18. Article
  19. Article
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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

6 authors at 1 institution in 1 country.

Yaqian ZhaoDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. zyq0926@126.com.
Guowei HuangDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. huangguowei@tmu.edu.cn.
Shuang ChenDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. chenshuang050109@126.com.
Yun GouDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. gou.yun1990@163.com.
Zhiping DongDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. dongjulia@163.com.
Xumei ZhangDepartment of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin 30070, China. zhangxumei@tmu.edu.cn.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated homocysteine (Hcy) levels have been reported to be involved in neurotoxicity after ischemic stroke. However, the underlying mechanisms remain incompletely understood to date. In the current study, we hypothesized that neuronal autophagy activation may be involved in the toxic effect of Hcy on cortical neurons following cerebral ischemia. Brain cell injury was determined by hematoxylin-eosin (HE) staining and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining. The level and localization of autophagy were detected by transmission electron microscopy, western blot and immunofluorescence double labeling. The oxidative DNA damage was revealed by immunofluorescence of 8-Hydroxy-2'-deoxyguanosine (8-OHdG). Hcy treatment aggravated neuronal cell death, significantly increased the formation of autophagosomes and the expression of LC3B and Beclin-1 in the brain cortex after middle cerebral artery occlusion-reperfusion (MCAO). Immunofluorescence analysis of LC3B and Beclin-1 distribution indicated that their expression occurred mainly in neurons (NeuN-positive) and hardly in astrocytes (GFAP-positive). 8-OHdG expression was also increased in the ischemic cortex of Hcy-treated animals. Conversely, LC3B and Beclin-1 overexpression and autophagosome accumulation caused by Hcy were partially blocked by the autophagy inhibitor 3-methyladenine (3-MA). Hcy administration enhanced neuronal autophagy, which contributes to cell death following cerebral ischemia. The oxidative damage-mediated autophagy may be a molecular mechanism underlying neuronal cell toxicity of elevated Hcy level.

Indexed as

AnimalsApoptosis Regulatory ProteinsAutophagyBlotting, WesternBrain IschemiaCerebral CortexFluorescent Antibody TechniqueHomocysteineInfarction, Middle Cerebral ArteryMaleNeuronsRatsRats, Sprague-DawleyReperfusion InjuryApoptosis Regulatory ProteinsHomocysteineautophagyhomocysteineneuronsoxidative stressreperfusion injury

Identifiers

PMID27455253
PMCPMC5000594
OpenAlexW2500152691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.