Evidence map›Paper›PMID 36587218›Full record

ArticleVirology journal2022

Mechanism of autophagy induced by activation of the AMPK/ERK/mTOR signaling pathway after TRIM22-mediated DENV-2 infection of HUVECs.

Ning Wu, Xiaoqin Gou, Pan Hu, Yao Chen, Jinzhong Ji, Yuanying Wang, Li Zuo

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  9. Multiple receptor tyrosine kinases regulate dengue infection of hepatocytes.Frontiers in cellular and infection microbiology · 2024
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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

7 authors at 1 institution in 1 country.

Ning WuChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Xiaoqin GouChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Pan HuChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Yao ChenChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Jinzhong JiChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Yuanying WangChemistry and Biochemistry Laboratory, Guizhou Medical University, Guiyang, China.
Li ZuoDepartment of Immunology, Guizhou Medical University, Guiyang, China. gzykdxzuoli@163.com.
Guiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDengue virus type 2 (DENV-2) was used to infect primary human umbilical vein endothelial cells (HUVECs) to examine autophagy induced by activation of the adenosine monophosphate-activated protein kinase (AMPK)/extracellular signal-regulated kinase (ERK)/mammalian target of rapamycin (mTOR) signaling pathway following tripartite motif-containing 22 (TRIM22)-mediated DENV-2 infection to further reveal the underlying pathogenic mechanism of DENV-2 infection.

methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was used to screen putative interference targets of TRIM22 and determine the knockdown efficiency. The effect of TRIM22 knockdown on HUVEC proliferation was determined using the CCK8 assay. Following TRIM22 knockdown, transmission electron microscopy (TEM) was used to determine the ultrastructure of HUVEC autophagosomes and expression of HUVEC autophagy and AMPK pathway-related genes were measured by qRT-PCR. Moreover, HUVEC autophagy and AMPK pathway-related protein expression levels were determined by western blot analysis. Cell cycle and apoptosis were assessed by flow cytometry (FCM) and the autophagosome structure of the HUVECs was observed by TEM.

resultsWestern blot results indicated that TRIM22 protein expression levels increased significantly 36 h after DENV-2 infection, which was consistent with the proteomics prediction. The CCK8 assay revealed that HUVEC proliferation was reduced following TRIM22 knockdown (P < 0.001). The TEM results indicated that HUVEC autolysosomes increased and autophagy was inhibited after TRIM22 knockdown. The qRT-PCR results revealed that after TRIM22 knockdown, the expression levels of antithymocyte globulin 7 (ATG7), antithymocyte globulin 5 (ATG5), Beclin1, ERK, and mTOR genes decreased (P < 0.01); however, the expression of AMPK genes (P < 0.05) and P62 genes (P < 0.001) increased. FCM revealed that following TRIM22 knockdown, the percentage of HUVECs in the G2 phase increased (P < 0.001) along with cell apoptosis. The effect of TRIM22 overexpression on HUVEC autophagy induced by DENV-2 infection and AMPK pathways decreased after adding an autophagy inhibitor.

conclusionsIn HUVECs, TRIM22 protein positively regulates autophagy and may affect autophagy through the AMPK/ERK/mTOR signaling pathway. Autophagy is induced by activation of the AMPK/ERK/mTOR signaling pathway following TRIM22-mediated DENV-2 infection of HUVECs.

Indexed as

AMP-Activated Protein KinasesExtracellular Signal-Regulated MAP KinasesAntilymphocyte SerumAutophagyHumansHuman Umbilical Vein Endothelial CellsMinor Histocompatibility AntigensRepressor ProteinsSignal TransductionSirolimusTOR Serine-Threonine KinasesTripartite Motif ProteinsAMP-Activated Protein KinasesAntilymphocyte SerumExtracellular Signal-Regulated MAP KinasesMinor Histocompatibility AntigensMTOR protein, humanRepressor ProteinsSirolimusTOR Serine-Threonine KinasesTRIM22 protein, humanTripartite Motif ProteinsAMPK/ERK/mTOR signaling pathwayAutophagyDENV-2TRIM22

Identifiers

PMID36587218
PMCPMC9805691
OpenAlexW4313394591

What OpenQuestion holds

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LicenceCC BY
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.