Evidence map›Paper›PMID 33269748›Full record

ArticleNeural regeneration research2021

TP53-induced glycolysis and apoptosis regulator alleviates hypoxia/ischemia-induced microglial pyroptosis and ischemic brain damage.

Lan-Lan Tan, Xiao-Lu Jiang, Li-Xiao Xu, Gen Li, Chen-Xi Feng, Xin Ding, Bin Sun, Zheng-Hong Qin, Zu-Bin Zhang, Xing Feng and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2021. 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
4.3field-weighted citation impact, top 4% 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, 69 citations in OpenAlex.

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  17. Neural regeneration research · 2023
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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

11 authors at 1 institution in 1 country.

Lan-Lan TanDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Xiao-Lu JiangDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Li-Xiao XuDepartment of Pediatrics Research Institute, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Gen LiDepartment of Pediatrics Research Institute, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Chen-Xi FengDepartment of Pediatrics Research Institute, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Xin DingDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Bin SunDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Zheng-Hong QinJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu Province, China.
Zu-Bin ZhangJiangsu Key Laboratory of Neuropsychiatric Diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu Province, China.
Xing FengDepartment of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Mei LiDepartment of Pediatrics Research Institute, Children's Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous studies have demonstrated that TP53-induced glycolysis and apoptosis regulator (TIGAR) can protect neurons after cerebral ischemia/reperfusion. However, the role of TIGAR in neonatal hypoxic-ischemic brain damage (HIBD) remains unknown. In the present study, 7-day-old Sprague-Dawley rat models of HIBD were established by permanent occlusion of the left common carotid artery followed by 2-hour hypoxia. At 6 days before induction of HIBD, a lentiviral vector containing short hairpin RNA of either TIGAR or gasdermin D (LV-sh_TIGAR or LV-sh_GSDMD) was injected into the left lateral ventricle and striatum. Highly aggressively proliferating immortalized (HAPI) microglial cell models of in vitro HIBD were established by 2-hour oxygen/glucose deprivation followed by 24-hour reoxygenation. Three days before in vitro HIBD induction, HAPI microglial cells were transfected with LV-sh_TIGAR or LV-sh_GSDMD. Our results showed that TIGAR expression was increased in the neonatal rat cortex after HIBD and in HAPI microglial cells after oxygen/glucose deprivation/reoxygenation. Lentivirus-mediated TIGAR knockdown in rats markedly worsened pyroptosis and brain damage after hypoxia/ischemia in vivo and in vitro. Application of exogenous nicotinamide adenine dinucleotide phosphate (NADPH) increased the NADPH level and the glutathione/oxidized glutathione ratio and decreased reactive oxygen species levels in HAPI microglial cells after oxygen/glucose deprivation/reoxygenation. Additionally, exogenous NADPH blocked the effects of TIGAR knockdown in neonatal HIBD in vivo and in vitro. These findings show that TIGAR can inhibit microglial pyroptosis and play a protective role in neonatal HIBD. The study was approved by the Animal Ethics Committee of Soochow University of China (approval No. 2017LW003) in 2017.

Indexed as

hypoxic-ischemic brain damagein vitroin vivomicrogliaNADPHpyroptosisROSTIGAR

Identifiers

PMID33269748
PMCPMC8224121
OpenAlexW3109678884

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.