Evidence map›Paper›PMID 29534734›Full record

ArticleMolecular brain2018

Vitamin A bio-modulates apoptosis via the mitochondrial pathway after hypoxic-ischemic brain damage.

Wei Jiang, Min Guo, Min Gong, Li Chen, Yang Bi, Yun Zhang, Yuan Shi, Ping Qu, Youxue Liu, Jie Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

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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.

Wei JiangChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Min GuoChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Min GongChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Li ChenChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yang BiChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yun ZhangChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yuan ShiChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Ping QuChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Youxue LiuChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Jie ChenChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. jchen010@foxmail.com.
Tingyu LiChildren Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. tyli@vip.sina.com.ORCID 0000-0002-1940-7076
China International Science and Technology Cooperation · CN

Funding

National Natural Science Foundation of China 30830106National Natural Science Foundation of China 81571091National Youth Foundation of China 81100454
6 · The paper itself

Abstract

Our previous studies demonstrated that vitamin A deficiency (VAD) can impair the postnatal cognitive function of rats by damaging the hippocampus. The present study examined the effects of retinoic acid (RA) on apoptosis induced by hypoxic-ischemic damage in vivo and in vitro, and investigated the possible signaling pathway involved in the neuroprotective anti-apoptotic effects of RA. Flow cytometry, immunofluorescence staining and behavioral tests were used to evaluate the neuroprotective and anti-apoptotic effects of RA. The protein and mRNA levels of RARα, PI3K, Akt, Bad, caspase-3, caspase-8, Bcl-2, Bax, and Bid were measured with western blotting and real-time PCR, respectively. We found impairments in learning and spatial memory in VAD group compared with vitamin A normal (VAN) and vitamin A supplemented (VAS) group. Additionally, we showed that hippocampal apoptosis was weaker in the VAN group than that in VAD group. Relative to the VAD group, the VAN group also had increased mRNA and protein levels of RARα and PI3K, and upregulated phosphorylated Akt/Bad levels in vivo. In vitro, excessively low or high RA signaling promoted apoptosis. Furthermore, the effects on apoptosis involved the mitochondrial membrane potential (MMP). These data support the idea that sustained VAD following hypoxic-ischemic brain damage (HIBD) inhibits RARα, which downregulates the PI3K/Akt/Bad and Bcl-2/Bax pathways and upregulates the caspase-8/Bid pathway to influence the MMP, ultimately producing deficits in learning and spatial memory in adolescence. This suggests that clinical interventions for HIBD should include suitable doses of VA.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCaspasesCells, CulturedDietary SupplementsFemaleGlucoseHippocampusHypoxia-Ischemia, BrainLearningMembrane Potential, MitochondrialMitochondriaNeuronsOxygenPhosphatidylinositol 3-Kinasesbcl-2-Associated X ProteinCaspasesGlucoseOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRetinoic Acid Receptor alphaRNA, MessengerTretinoinVitamin AApoptosisHypoxic-ischemic brain damage (HIBD)Mitochondrial membrane potential (MMP)PI3K/AktRetinoic acid (RA)Vitamin A (VA)

Identifiers

PMID29534734
PMCPMC5851324
OpenAlexW2801128669

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.