Evidence map›Paper›PMID 35970046›Full record

ArticleBiochemical and biophysical research communications2022

SARS-CoV-2 spike S1 subunit protein-mediated increase of beta-secretase 1 (BACE1) impairs human brain vessel cells.

Ji-Young Choi, Jung Hyun Park, Chulman Jo, Kyung-Chang Kim, Young Ho Koh

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Cerebrovascular Endothelial Dysfunction: Role of BACE1.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  7. Article
  8. The neurobiology of SARS-CoV-2 infection.Nature reviews. Neuroscience · 2024
    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

5 authors.

Ji-Young ChoiDivision of Brain Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju-si, Chungcheongbuk-do, 28159, South Korea.
Jung Hyun ParkDivision of Brain Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju-si, Chungcheongbuk-do, 28159, South Korea.
Chulman JoDivision of Brain Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju-si, Chungcheongbuk-do, 28159, South Korea.
Kyung-Chang KimDivision of Emerging Virus and Vector Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheongju-si, Chungchengbuk-do, 28159, South Korea.
Young Ho KohDivision of Brain Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Cheongju-si, Chungcheongbuk-do, 28159, South Korea. Electronic address: kohyoungho122@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence suggests incomplete recovery of COVID-19 patients, who continue to suffer from cardiovascular diseases, including cerebral vascular disorders (CVD) and neurological symptoms. Recent findings indicate that some of the damaging effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, especially in the brain, may be induced by the spike protein, leading to the disruption of the initial blood-brain barrier (BBB). SARS-CoV-2-infected cells and animals exhibit age-dependent pathogenesis. In this study, we identified endothelial BACE1 as a critical mediator of BBB disruption and cellular senescence induced by the SARS-CoV-2 spike S1 subunit protein. Increased BACE1 in human brain microvascular endothelial cells (HBMVEC) decreases the levels of tight junction proteins, including ZO-1, occludin, and claudins. Moreover, BACE1 overexpression leads to the accumulation of p16 and p21, typical hallmarks of cellular senescence. Our findings show that the SARS-CoV-2 spike S1 subunit protein upregulated BACE1 expression in HBMVECs, causing endothelial leakage. In addition, the SARS-CoV-2 spike S1 subunit protein induced p16 and p21 expression, indicating BACE1-mediated cellular senescence, confirmed by β-Gal staining in HBMVECs. In conclusion, this study demonstrated that BACE1-mediated endothelial cell damage and senescence may be linked to CVD after COVID-19 infection.

Indexed as

Cardiovascular DiseasesCOVID-19Amyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBrainEndothelial CellsHumansSARS-CoV-2Spike Glycoprotein, CoronavirusAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2BACE1Brain vesselsCell senescenceCOVID-19SARS-CoV-2

Identifiers

PMID35970046
PMCPMC9349051

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.