Evidence map›Paper›PMID 36096380›Full record

ArticleMolecular and cellular endocrinology2022

Overexpression of estrogen receptor GPER1 and G1 treatment reduces SARS-CoV-2 infection in BEAS-2B bronchial cells.

Angelica Jardim Costa, Robertha Mariana Rodrigues Lemes, Cynthia Silva Bartolomeo, Tamires Alves Nunes, Gabriela Cruz Pereira, Rafaela Brito Oliveira, Alexandre Lopes Gomes, Soraya Soubhi Smaili, Rui Monteiro de Barros Maciel, Louise Newson and 5 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 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
2.2field-weighted citation impact, top 12% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Estrogen and viral infection.Frontiers in immunology · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. 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

15 authors at 5 institutions in 1 country.

Angelica Jardim CostaUniversidade Federal de São Paulo, Escola Paulista de Medicina, Department of Pharmacology, São Paulo, SP, Brazil.
Robertha Mariana Rodrigues LemesUniversidade Federal de São Paulo, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Department of Biological Sciences, Diadema, SP, Brazil; Universidade Federal de São Paulo, Escola Paulista de Medicina, Laboratory of Molecular and Translational Endocrinology, São Paulo, SP, Brazil.
Cynthia Silva BartolomeoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil; Universidade Federal de São Paulo, Instituto de Saúde e Sociedade, Departament of Biosciences, Santos, SP, Brazil.
Tamires Alves NunesDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil; Universidade Federal de São Paulo, Instituto de Saúde e Sociedade, Departament of Biosciences, Santos, SP, Brazil.
Gabriela Cruz PereiraUniversidade Federal de São Paulo, Escola Paulista de Medicina, Department of Biochemistry, São Paulo, SP, Brazil.
Rafaela Brito OliveiraUniversidade Federal de São Paulo, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Department of Biological Sciences, Diadema, SP, Brazil; Universidade Federal de São Paulo, Escola Paulista de Medicina, Laboratory of Molecular and Translational Endocrinology, São Paulo, SP, Brazil.
Alexandre Lopes GomesInstituto Biológico, Secretaria de Agricultura e Abastecimento, São Paulo, SP, Brazil.
Soraya Soubhi SmailiUniversidade Federal de São Paulo, Escola Paulista de Medicina, Department of Pharmacology, São Paulo, SP, Brazil.
Rui Monteiro de Barros MacielUniversidade Federal de São Paulo, Escola Paulista de Medicina, Laboratory of Molecular and Translational Endocrinology, São Paulo, SP, Brazil; Universidade Federal de São Paulo, Escola Paulista de Medicina, Department of Medicine, São Paulo, SP, Brazil.
Louise NewsonNewson Health Research and Education, Stratford-Upon-Avon, UK.
Ana Lopez RamirezCambridge Institute for Medical Research, Cambridge, UK.
Liria Hiromi OkudaInstituto Biológico, Secretaria de Agricultura e Abastecimento, São Paulo, SP, Brazil.
Carla Máximo PradoUniversidade Federal de São Paulo, Instituto de Saúde e Sociedade, Departament of Biosciences, Santos, SP, Brazil.
Roberta Sessa StilhanoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil.
Rodrigo Portes UreshinoUniversidade Federal de São Paulo, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Department of Biological Sciences, Diadema, SP, Brazil; Universidade Federal de São Paulo, Escola Paulista de Medicina, Laboratory of Molecular and Translational Endocrinology, São Paulo, SP, Brazil. Electronic address: rpureshino@gmail.com.
Universidade Federal de São Paulo · BRFaculdade de Ciências Médicas da Santa Casa de São Paulo · BRInstituto de Ciências Farmacêuticas · BRInstituto Biológico · BRInstituto de Saúde · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gender-bias in COVID-19 severity has been suggested by clinical data. Experimental data in cell and animal models have demonstrated the role of sex hormones, particularly estrogens, in viral infections such as in COVID-19. SARS-CoV-2 uses ACE2 as a receptor to recognize host cells, and the protease TMPRSS2 for priming the Spike protein, facilitating virus entry into cells. However, the involvement of estrogenic receptors in SARS-CoV-2 infection are still being explored. Thus, in order to investigate the role of estrogen and its receptors in COVID-19, the estrogen receptors ERα, ERβ and GPER1 were overexpressed in bronchial BEAS-2B cell, and then infected with SARS-CoV-2. Interestingly, the levels of ACE2 and TMPRSS2 mRNA were higher in SARS-CoV-2-infected cells, but no difference was observed in cells with estrogen receptors overexpression. GPER1 can be involved in virus infection or replication, since its higher levels reduces SARS-CoV-2 load. On the other hand, pharmacological antagonism of GPER1 enhanced viral load. Those data suggest that GPER1 has an important role in SARS-CoV-2 infection.

Indexed as

COVID-19Angiotensin-Converting Enzyme 2AnimalsEstrogen Receptor alphaEstrogen Receptor betaEstrogensPeptidyl-Dipeptidase AReceptors, EstrogenRNA, MessengerSARS-CoV-2Spike Glycoprotein, CoronavirusAngiotensin-Converting Enzyme 2Estrogen Receptor alphaEstrogen Receptor betaEstrogensPeptidyl-Dipeptidase AReceptors, EstrogenRNA, MessengerSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2BEAS-2BCOVID-19Estrogen receptorsGenderGPER1

Identifiers

PMID36096380
PMCPMC9458763
OpenAlexW4295021210

What Socratic holds

Textmetadata
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.