Evidence map›Paper›PMID 34070407›Full record

ArticleMicroorganisms2021

Human Cytomegalovirus Reduces Endothelin-1 Expression in Both Endothelial and Vascular Smooth Muscle Cells.

Koon-Chu Yaiw, Abdul-Aleem Mohammad, Chato Taher, Huanhuan Leah Cui, Helena Costa, Ourania N Kostopoulou, Masany Jung, Alice Assinger, Vanessa Wilhelmi, Jiangning Yang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Microorganisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 9 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

14 authors at 3 institutions in 2 countries.

Koon-Chu YaiwDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Abdul-Aleem MohammadDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Chato TaherDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Huanhuan Leah CuiDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Helena CostaDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Ourania N KostopoulouDepartment of Oncology and Pathology, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Masany JungDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Alice AssingerInstitute of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, A-1090 Vienna, Austria.ORCID 0000-0002-5670-5910
Vanessa WilhelmiDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Jiangning YangDepartment of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital Solna, SE 171 64 Stockholm, Sweden.
Klas StrååtDepartment of Medicine, Division of Hematology, BioClinicum and Centre for Molecular Medicine, Karolinska University, Hospital Solna and Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Afsar RahbarDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
John PernowDepartment of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital Solna, SE 171 64 Stockholm, Sweden.
Cecilia Söderberg-NauclérDepartment of Medicine, Solna, Microbial Pathogenesis Unit, Karolinska Institutet, SE 171 64 Stockholm, Sweden.
Karolinska University Hospital · SEKarolinska Institutet · SEMedical University of Vienna · AT

Funding

Swedish Cancer Foundation 5044-B05-01XABVetenskapsrådet 10350, K2014-99X-22627-01-4, K2013-57X-12615-16-5 and K2013-54X-20324-07-5)
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is an opportunistic pathogen that has been implicated in the pathogenesis of atherosclerosis. Endothelin-1 (ET-1), a potent vasoconstrictive peptide, is overexpressed and strongly associated with many vasculopathies. The main objective of this study was to investigate whether HCMV could affect ET-1 production. As such, both endothelial and smooth muscle cells, two primary cell types involved in the pathogenesis of atherosclerosis, were infected with HCMV in vitro and ET-1 mRNA and proteins were assessed by quantitative PCR assay, immunofluorescence staining and ELISA. HCMV infection significantly decreased ET-1 mRNA and secreted bioactive ET-1 levels from both cell types and promoted accumulation of the ET-1 precursor protein in infected endothelial cells. This was associated with inhibition of expression of the endothelin converting enzyme-1 (ECE-1), which cleaves the ET-1 precursor protein to mature ET-1. Ganciclovir treatment did not prevent the virus suppressive effects on ET-1 expression. Consistent with this observation we identified that the IE2-p86 protein predominantly modulated ET-1 expression. Whether the pronounced effects of HCMV in reducing ET-1 expression in vitro may lead to consequences for regulation of the vascular tone in vivo remains to be proven.

Indexed as

endothelial cellsendothelin-1human cytomegalovirusimmediate-earlysmooth muscle cells

Identifiers

PMID34070407
PMCPMC8229579
OpenAlexW3165150661

What Socratic holds

Textmetadata
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 Socratic graph.