Evidence map›Paper›PMID 27488808›Full record

ArticleScientific reports2016

Hypoxic Preconditioning Inhibits Hypoxia-induced Apoptosis of Cardiac Progenitor Cells via the PI3K/Akt-DNMT1-p53 Pathway.

Rongfeng Xu, Yuning Sun, Zhongpu Chen, Yuyu Yao, Genshan Ma

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-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

24 citing papers in PubMed, 50 citations in OpenAlex.

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  18. Genome-wide DNA methylation encodes cardiac transcriptional reprogramming in human ischemic heart failure.Laboratory investigation; a journal of technical methods and pathology · 2019
    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

5 authors at 1 institution in 1 country.

Rongfeng XuDepartment of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, Jiangsu, China.
Yuning SunDepartment of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, Jiangsu, China.
Zhongpu ChenDepartment of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, Jiangsu, China.
Yuyu YaoDepartment of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, Jiangsu, China.
Genshan MaDepartment of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, Jiangsu, China.
Zhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Research has demonstrated that hypoxic preconditioning (HP) can enhance the survival and proliferation of cardiac progenitor cells (CPCs); however, the underlying mechanisms are not fully understood. Here, we report that HP of c-kit (+) CPCs inhibits p53 via the PI3K/Akt-DNMT1 pathway. First, CPCs were isolated from the hearts of C57BL/6 mice and further purified by magnetic-activated cell sorting. Next, these cells were cultured under either normoxia (H0) or HP for 6 hours (H6) followed by oxygen-serum deprivation for 24 hours (24h). Flow cytometric analysis and MTT assays revealed that hypoxia-preconditioned CPCs exhibited an increased survival rate. Western blot and quantitative real-time PCR assays showed that p53 was obviously inhibited, while DNMT1 and DNMT3β were both significantly up-regulated by HP. Bisulphite sequencing analysis indicated that DNMT1 and DNMT3β did not cause p53 promoter hypermethylation. A reporter gene assay and chromatin immunoprecipitation analysis further demonstrated that DNMT1 bound to the promoter locus of p53 in hypoxia-preconditioned CPCs. Together, these observations suggest that HP of CPCs could lead to p53 inhibition by up-regulating DNMT1 and DNMT3β, which does not result in p53 promoter hypermethylation, and that DNMT1 might directly repress p53, at least in part, by binding to the p53 promoter locus.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsApoptosisCell ProliferationCells, CulturedDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationHypoxiaMiceMice, Inbred C57BLMyoblasts, CardiacOncogene Protein v-aktPhosphatidylinositol 3-KinasesPromoter Regions, GeneticTumor Suppressor Protein p53DNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, mouseOncogene Protein v-aktPhosphatidylinositol 3-KinasesTumor Suppressor Protein p53

Identifiers

PMID27488808
PMCPMC4973228
OpenAlexW2479740076

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Registered trials

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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.