Evidence map›Paper›PMID 32124933›Full record

ArticleInternational journal of molecular medicine2020

HIF‑1α attenuates neuronal apoptosis by upregulating EPO expression following cerebral ischemia‑reperfusion injury in a rat MCAO model.

Jun Li, Tao Tao, Jian Xu, Zhi Liu, Zhehua Zou, Minglu Jin

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.4field-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

40 citing papers in PubMed, 42 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

6 authors at 5 institutions in 1 country.

Jun LiDepartment of Rehabilitation Medicine, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Tao TaoDepartment of Rehabilitation Medicine, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Jian XuDepartment of Neurology, The Affiliated Hospital Guizhou Medical University, Guiyang, Guizhou 550001, P.R. China.
Zhi LiuDepartment of Pharmacy, The Affiliated Hospital Guizhou Medical University, Guiyang, Guizhou 550001, P.R. China.
Zhehua ZouDepartment of General Practice, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei 066000, P.R. China.
Minglu JinDepartment of Neurology, Qijiang Hospital of The First Affiliated Hospital of Chongqing Medical University, Chongqing 404100, P.R. China.
Guizhou Provincial People's Hospital · CNAffiliated Hospital of Guizhou Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNFirst Hospital of Qinhuangdao · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia‑inducible factor‑1α (HIF‑1α) is a key transcriptional factor in response to hypoxia and is involved in ischemic stroke. In the present study, the potential for HIF‑1α to inhibit neuronal apoptosis through upregulating erythropoietin (EPO) was investigated in a transient middle cerebral artery occlusion (tMCAO) rat stroke model. For this purpose, a recombinant adenovirus expressing HIF‑1α was engineered (Ad‑HIF‑1α). Control adenovirus (Ad group), Ad‑HIF‑1α (Ad‑HIF‑1α group) or Ad‑HIF‑1α in addition to erythropoietin mimetic peptide‑9 (EMP9), an EPO‑receptor (‑R) antagonist (Ad‑HIF‑1α+EMP9 group), were used for an intracranial injection into rat ischemic penumbra 1 h following MCAO. All rats demonstrated functional improvement following tMCAO, while the improvement rate was faster in rats treated by Ad‑HIF‑1α compared with all other groups. The EPO‑R inhibitor partially reversed the benefits of Ad‑HIF‑1α. Apoptosis induced by tMCAO was significantly inhibited by Ad‑HIF‑1α (P<0.05). The expression of HIF‑1α, evaluated by immunohistochemistry either in neurons or astrocytes, was upregulated by Ad‑HIF‑1α. Both EPO mRNA and protein expression were increased by Ad‑HIF‑1α, however, there was no significant change of EPO‑R either on an mRNA level or protein level. Furthermore, EMP9 did not change the EPO expression which was upregulated by Ad‑HIF‑1α. Activated caspase 3 in neurons was suppressed by Ad‑HIF‑1α. Activated caspase 3 downregulated by HIF‑1α was partially blocked by EMP9. Altogether, the present data demonstrated that HIF‑1α attenuates neuronal apoptosis partially through upregulating EPO following cerebral ischemia in rat. Thus, upregulating HIF‑1α subsequent to a stroke may be a potential treatment for ischemic stroke.

Indexed as

ApoptosisGene Expression RegulationAnimalsBrain DiseasesDisease Models, AnimalErythropoietinHypoxia-Inducible Factor 1, alpha SubunitMaleNeuronsRatsRats, Sprague-DawleyReperfusion InjuryErythropoietinerythropoietin, ratHif1a protein, ratHypoxia-Inducible Factor 1, alpha Subunit

Identifiers

PMID32124933
PMCPMC7053873
OpenAlexW3004055982

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.