Evidence map›Paper›PMID 32694928›Full record

ArticleMediators of inflammation2020

A Novel Putative Role of TNK1 in Atherosclerotic Inflammation Implicating the Tyk2/STAT1 Pathway.

Mei-Hua Bao, Qiao-Li Lv, Hai-Gang Li, Yi-Wen Zhang, Bao-Feng Xu, Bin-Sheng He

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
0.2field-weighted citation impact, top 47% 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, 2 syntheses or guidelines pooled it, 30 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 4 institutions in 1 country.

Mei-Hua Bao *Academician Workstation, Changsha Medical University, Changsha 410219, China.ORCID https://orcid.org/0000-0003-4784-7076
Qiao-Li Lv *Department of Science and Education, Jiangxi Key Laboratory of Translational Cancer Research, Jiangxi Cancer Hospital, 519 Beijing East Road, Nanchang, Jiangxi 330029, China.
Hai-Gang LiAcademician Workstation, Changsha Medical University, Changsha 410219, China.
Yi-Wen ZhangDepartment of Pharmacy, Zhejiang Provincial People's Hospital of Hangzhou Medical College, Hangzhou 310010, China.
Bao-Feng XuDepartment of Neurosurgery, the First Hospital of Jilin University, Changchun 130021, China.ORCID https://orcid.org/0000-0002-2764-7985
Bin-Sheng HeAcademician Workstation, Changsha Medical University, Changsha 410219, China.ORCID https://orcid.org/0000-0002-2232-4634
Changsha Medical University · CNJiangxi Provincial Cancer Hospital · CNJilin University · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAtherosclerosis is a chronic inflammatory disease which is responsible for many clinical manifestations. The present study was to investigate the anti-inflammatory functions and mechanisms of TNK1 in atherosclerosis.

methodsThe ApoE(-/-) mice and human carotid endarterectomy (CEA) atherosclerotic plaques were used to investigate the differential expression of TNK1. The ApoE(-/-) mice were fed with high-fat diet (HFD) or normal-fat diet (NFD) for 8 weeks; the aorta was separated and stained with oil red O to evaluate the formation of atherosclerosis. TNK1 in mice aorta was measured by qPCR. The human CEA were obtained and identified as ruptured and stable plaques. The level of TNK1 was measured by qPCR and Western-blot staining. Further studies were conducted in THP-1 cells to explore the anti-inflammatory effects of TNK1. We induced the formation of macrophages by incubating THP-1 cells with PMA (phorbol 12-myristate 13-acetate). Afterwards, oxidized low-density lipoprotein (oxLDL) was used to stimulate the inflammation, and the secretion of inflammatory factors was measured by ELISA and qPCR. The levels of TNK1, total STAT1 and Tyk2, and the phosphorylation of STAT1 and Tyk2 were measured by western blot to uncover the mechanisms of TNK1.

resultsThe oil red O staining indicated obvious deposition of lipid on the aorta of ApoE(-/-) mice after 8-week HFD treatment. The TNK1 level was much higher in both the HFD-fed ApoE(-/-) mice aorta arch and the ruptured human CEA plaques. We found that TNK1 was highly expressed in THP-1 cells, compared to other atherosclerotic related cells (HUVEC, HBMEC, and HA-VSMC), indicating TNK1 might be involved in the inflammation. Suppressing the expression of TNK1 by shTNK1 inhibited the oxLDL-induced secretion of inflammatory factors, such as IL-12, IL-6, and TNF-

conclusionTNK1 participated in the inflammation in atherosclerosis. shTNK1 suppressed the oxLDL-induced inflammation and lipid deposition in THP-1 cells. The mechanism might be related to the Tyk2/STAT signal pathway.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBlotting, WesternEnzyme-Linked Immunosorbent AssayHumansInflammationMaleMicePlaque, AtheroscleroticProtein-Tyrosine KinasesSTAT1 Transcription FactorTHP-1 CellsTYK2 KinaseApolipoproteins EKos1 protein, mouseProtein-Tyrosine KinasesStat1 protein, mouseSTAT1 Transcription FactorTYK2 KinaseTyk2 protein, mouse

Identifiers

PMID32694928
PMCPMC7368939
OpenAlexW3041041773

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.