Evidence map›Paper›PMID 34218417›Full record

ArticleMolecular neurobiology2021

SETD3 Downregulation Mediates PTEN Upregulation-Induced Ischemic Neuronal Death Through Suppression of Actin Polymerization and Mitochondrial Function.

Xiangyu Xu, Yu Cui, Congqin Li, Yuyang Wang, Jing Cheng, Songfeng Chen, Jiangdong Sun, Jinyang Ren, Xujin Yao, Jingchen Gao and 3 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Neuroprotective effects of phenylacetylglycine via β2AR on cerebral ischemia/reperfusion injury in rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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  7. IRF-1-inhibited lncRNA XIST regulated the osteogenic differentiation via miR-450b/FBXW7 axis.Apoptosis : an international journal on programmed cell death · 2023
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  11. Review
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 2 institutions in 1 country.

Xiangyu Xu *Department of Rehabilitation, Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Yu Cui *Institute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Congqin LiDepartment of Rehabilitation, Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Yuyang WangDepartment of Rehabilitation, Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Jing ChengDepartment of Physiology, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, 430071, China.
Songfeng ChenDepartment of Physiology, School of Medicine, Wuhan University, 185 Donghu Street, Wuhan, 430071, China.
Jiangdong SunInstitute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Jinyang RenInstitute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Xujin YaoInstitute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Jingchen GaoInstitute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Xiaohong HuangInstitute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Qi Wan *Institute of Neuroregeneration & Neurorehabilitation, Department of Pathophysiology, Qingdao University, Qingdao, 266071, China.
Qiang Wang *Department of Rehabilitation, Affiliated Hospital of Qingdao University, Qingdao, 266000, China. sakulawangqiang@hotmail.com.ORCID http://orcid.org/0000-0001-7775-3375
Qingdao University · CNWuhan University · CN

Funding

Clinical Medicine +X grant of the Affiliated Hospital of Qingdao University QDFY+X2019005National Key R&D Program of China 2019YFC0120000; 2018YFC1312300National Natural Science Foundation of China 31900634Natural Science Foundation of Shandong Province (CN) ZR2020MH282the Key Research and Development Project of Shandong 2019JZZY021010the National Natural Science Foundation of China NSFC: 82071385
6 · The paper itself

Abstract

SET domain protein 3 (SETD3) is an actin-specific methyltransferase, a rare post-translational modification with limited known biological functions. Till now, the function of SETD3 in cerebral ischemia-reperfusion (I/R)-induced injury remains unknown. Here, we show that the protein level of SETD3 is decreased in rat neurons after cerebral I/R injury. SETD3 promotes neuronal survival after both glucose and oxygen deprivation/reoxygenation (OGD/R) and cerebral I/R injury, and knockdown of SETD3 increases OGD/R-induced neuronal death. We further show that OGD/R-induced downregulation of SETD3 leads to the decrease of cellular ATP level, the reduction of mitochondrial electric potential and the increase of ROS production, thereby promoting mitochondrial dysfunction. We found that SETD3 reduction-induced mitochondrial dysfunction is mediated by the suppression of actin polymerization after OGD/R. Furthermore, we demonstrate that I/R-induced upregulation of PTEN leads to the downregulation of SETD3, and suppressing PTEN protects against ischemic neuronal death through downregulation of SETD3 and enhancement of actin polymerization. Together, this study provides the first evidence suggesting that I/R-induced downregulation of SETD3 mediates PTEN upregulation-induced ischemic neuronal death through downregulation of SETD3 and subsequent suppression of actin polymerization. Thus, upregulating SETD3 is a potential approach for the development of ischemic stroke therapy.

Indexed as

ActinsAnimalsBrain IschemiaCell DeathCells, CulturedDown-RegulationFemaleHistone MethyltransferasesMaleMitochondriaNeuronsPolymerizationPTEN PhosphohydrolaseRatsRats, Sprague-DawleyReperfusion InjuryActinsHistone MethyltransferasesPTEN PhosphohydrolasePten protein, ratRNA, Small InterferingSetd3 protein, mouseActin polymerizationIschemia-reperfusion injuryMitochondrial functionSETD3

Identifiers

PMID34218417
OpenAlexW3178756715

What OpenQuestion holds

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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.