Evidence map›Paper›PMID 28656218›Full record

ArticleMolecular medicine reports2017

Investigation of highly expressed PCSK9 in atherosclerotic plaques and ox-LDL-induced endothelial cell apoptosis.

Jiao Li, Xue Liang, Yuanyuan Wang, Zhao Xu, Guangping Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

44 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  20. The Anti-Thrombotic Effects of PCSK9 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2023
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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

5 authors.

Jiao LiTianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Xue LiangTianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Yuanyuan WangTianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Zhao XuTianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.
Guangping LiTianjin Key Laboratory of Ionic‑Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to explore the direct toxicity of proprotein convertase subtilisin/kexin type 9 (PCSK9) to atherosclerosis (AS) and its association with apoptotic endothelial cells. Apolipoprotein E‑/‑ mice were randomly divided into two groups, control and experimental. The control group was administered a normal diet and the experimental group was administered a high‑fat diet. After 20 weeks, the aorta was isolated and dissected. Hematoxylin and eosin staining, and immunohistochemical analysis were performed. Human umbilical vein endothelial cells were incubated with varied concentrations of oxidized low‑density lipoprotein (ox‑LDL) for different times. The apoptotic rate was detected by flow cytometry. Western blotting and reverse transcription‑quantitative polymerase chain reaction analysis were conducted to detect the expression of PCSK9, B‑cell lymphoma 2 (Bcl‑2), bcl‑2‑like protein 4 (Bax) and caspase-3. Short hairpin (sh) RNA‑PCSK9 was transfected into endothelial cells using lentiviral transfection. The expression levels of PCSK9, Bax, Bcl‑2, caspase-3 and the mitogen‑activated protein kinase (MAPK) pathway proteins were detected. The high‑fat group was successfully established as an AS model and PCSK9 was highly expressed in the AS plaque. Treatment with ox‑LDL induced apoptosis and increased mRNA and protein levels of PCSK9. PCSK9 mRNA and proteins levels were downregulated by shRNA‑PCSK9. The deficiency of PCSK9 markedly inhibited the expression of pro‑apoptotic proteins and promoted anti‑apoptotic proteins. In addition, phosphorylation of p38 and c‑Jun N‑terminal kinases was altered by shRNA‑PCSK9. Targeting of PCSK9 by shRNA‑PCSK9 may repress endothelial cell apoptosis through MAPK signaling in AS, providing a novel direction for understanding the mechanism and treatment of AS.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCaspase 3Disease Models, AnimalDown-RegulationHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLMAP Kinase Signaling SystemMicePlaque, AtheroscleroticProprotein Convertase 9RNA, Small InterferingTransfectionUp-Regulationbcl-2-Associated X ProteinCaspase 3Lipoproteins, LDLoxidized low density lipoproteinProprotein Convertase 9RNA, Small Interfering

Identifiers

PMID28656218
PMCPMC5561783

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.