Evidence map›Paper›PMID 33317626›Full record

ArticleStem cell research & therapy2020

ELABELA ameliorates hypoxic/ischemic-induced bone mesenchymal stem cell apoptosis via alleviation of mitochondrial dysfunction and activation of PI3K/AKT and ERK1/2 pathways.

Jiaying Fu, Xuxiang Chen, Xin Liu, Daishi Xu, Huan Yang, Chaotao Zeng, Huibao Long, Changqing Zhou, Haidong Wu, Guanghui Zheng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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  20. Frontiers in veterinary science · 2022
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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

13 authors at 3 institutions in 1 country.

Jiaying FuDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Xuxiang ChenDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Xin LiuDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Daishi XuDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Huan YangDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Chaotao ZengDepartment of Emergency, the Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510120, Guangdong, People's Republic of China.
Huibao LongDepartment of Emergency, the Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510120, Guangdong, People's Republic of China.
Changqing ZhouDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Haidong WuDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Guanghui ZhengDepartment of Emergency, the Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510120, Guangdong, People's Republic of China.
Hao WuDepartment of Emergency, the Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510120, Guangdong, People's Republic of China.
Wuming WangDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China.
Tong WangDepartment of Emergency, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518033, Guangdong, People's Republic of China. tongwang316@163.com.
Sun Yat-sen University · CNEighth Affiliated Hospital of Sun Yat-sen UniversitySun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stem cells (MSCs) have exerted their brilliant potential to promote heart repair following myocardial infarction. However, low survival rate of MSCs after transplantation due to harsh conditions with hypoxic and ischemic stress limits their therapeutic efficiency in treating cardiac dysfunction. ELABELA (ELA) serves as a peptide hormone which has been proved to facilitate cell growth, survival, and pluripotency in human embryonic stem cells. Although ELA works as an endogenous ligand of a G protein-coupled receptor APJ (Apelin receptor, APLNR), whether APJ is an essential signal for the function of ELA remains elusive. The effect of ELA on apoptosis of MSCs is still vague.

objectiveWe studied the role of ELABELA (ELA) treatment on the anti-apoptosis of MSCs in hypoxic/ischemic (H/I) conditions which mimic the impaired myocardial microenvironment and explored the possible mechanisms in vitro.

methodsMSCs were obtained from donated rats weighing between 80~120 g. MSCs were exposed to serum-free and hypoxic (1% O

resultsWe found that ELA treatment of H/I-induced MSCs improved overall cell viability, enhanced Bcl/Bax expression, and decreased Caspase 3 activity. ELA inhibited H/I-induced mitochondrial dysfunction by increasing ATP concentration and suppressing the loss of mitochondrial transmembrane potential. However, this anti-apoptotic property of ELA was restrained in APJ-silenced MSCs. Additionally, ELA treatment induced the phosphorylation of AKT and ERK, while the blockade of PI3K/AKT and ERK1/2 pathways with respective inhibitors, LY294002 and U0126, suppressed the action of ELA.

conclusionELA positively affected on the survival of MSCs and exhibited anti-apoptotic characteristics when exposed to hypoxic/ischemic condition in vitro. Also, the function of ELA was correlated with the APJ receptor, reduced mitochondrial damage, and activation of the PI3K/AKT and ERK1/2 signal axes.

Indexed as

MAP Kinase Signaling SystemMesenchymal Stem CellsAnimalsApoptosisMitochondriaPeptide HormonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsLOC100912649 protein, ratPeptide HormonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisELABELAHypoxic/ischemicMesenchymal stem cellsPutative receptor protein related to the angiotensin receptor AT1 endogenous ligand

Identifiers

PMID33317626
PMCPMC7734864
OpenAlexW3111761623

What OpenQuestion holds

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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.