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3 results on '"Rui Monteiro, de Barros Maciel"'

1. 17β‐estradiol reduces SARS‐CoV‐2 infection in vitro

Author

Robertha Mariana Rodrigues Lemes, Angelica Jardim Costa, Cynthia Silva Bartolomeo, Taysa Bervian Bassani, Michelle Sayuri Nishino, Gustavo Jose da Silva Pereira, Soraya Soubhi Smaili, Rui Monteiro de Barros Maciel, Carla Torres Braconi, Edgar Ferreira da Cruz, Ana Lopez Ramirez, Juliana Terzi Maricatto, Luiz Mario Ramos Janini, Carla Máximo Prado, Roberta Sessa Stilhano, and Rodrigo Portes Ureshino

Subjects
17β‐estradiol, COVID‐19, estrogen receptors, gender, SARS‐CoV‐2, VERO E6 cells, Physiology, QP1-981
Abstract

Abstract The COVID‐19 has originated from Wuhan, China, in December 2019 and has been affecting the public health system, society, and economy in an unheard‐of manner. There is no specific treatment or vaccine available for COVID‐19. Previous data showed that men are more affected than women by COVID‐19, then we hypothesized whether sex hormones could be protecting the female organism against the infection. VERO E6 cells have been commonly used as in vitro model for SARS‐CoV‐2 infection. In our experimental approach, we have treated VERO E6 cells with 17β‐estradiol to evaluate the modulation of SARS‐CoV‐2 infection in this cell line. Here we demonstrated that estrogen protein receptors ERα, ERβ, and GPER1 are expressed by VERO E6 cells and could be used to study the effects of this steroid hormone. Previous and 24‐hours post‐infection, cells treated with 17β‐estradiol revealed a reduction in the viral load. Afterward, we found that SARS‐CoV‐2 infection per se results in ACE2 and TMPRSS2 increased gene expression in VERO E6‐cell, which could be generating a cycle of virus infection in host cells. The estrogen treatment reduces the levels of the TMPRSS2, which are involved with SARS‐CoV‐2 infectiveness capacity, and hence, reducing the pathogenicity/genesis. These data suggest that estrogen could be a potential therapeutic target promoting cell protection against SARS‐CoV‐2. This opens new possibilities for further studies on 17β‐estradiol in human cell lines infected by SARS‐CoV‐2 and at least in part, explain why men developed a more severe COVID‐19 compared to women.

Published
2021
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2. Overexpression of estrogen receptor GPER1 and G1 treatment reduces SARS-CoV-2 infection in BEAS-2B bronchial cells

Author

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, Ana Lopez Ramirez, Liria Hiromi Okuda, Carla Máximo Prado, Roberta Sessa Stilhano, and Rodrigo Portes Ureshino

Subjects
SARS-CoV-2, Estrogen Receptor alpha, COVID-19, Estrogens, Peptidyl-Dipeptidase A, Biochemistry, Endocrinology, Receptors, Estrogen, Spike Glycoprotein, Coronavirus, Animals, Estrogen Receptor beta, Angiotensin-Converting Enzyme 2, RNA, Messenger, Molecular Biology
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.

Published
2022

3. SARS-CoV-2 infection and replication kinetics in different human cell types: The role of autophagy, cellular metabolism and ACE2 expression

Author

Cynthia Silva, Bartolomeo, Robertha Mariana Rodrigues, Lemes, Rafael Leite, Morais, Gabriela Cruz, Pereria, Tamires Alves, Nunes, Angelica Jardim, Costa, Rui Monteiro, de Barros Maciel, Carla Torres, Braconi, Juliana Terzi, Maricato, Luiz Mario Ramos, Janini, Liria Hiromi, Okuda, Kil Sun, Lee, Carla Máximo, Prado, Rodrigo Portes, Ureshino, and Roberta Sessa, Stilhano

Subjects
SARS-CoV-2, COVID-19, Citrate (si)-Synthase, General Medicine, Peptidyl-Dipeptidase A, General Biochemistry, Genetics and Molecular Biology, Neuroblastoma, Adenosine Triphosphate, HEK293 Cells, Autophagy, Humans, Angiotensin-Converting Enzyme 2, RNA, Messenger, Caco-2 Cells, General Pharmacology, Toxicology and Pharmaceutics
Abstract

This study evaluated SARS-CoV-2 replication in human cell lines derived from various tissues and investigated molecular mechanisms related to viral infection susceptibility and replication.SARS-CoV-2 replication in BEAS-2B and A549 (respiratory tract), HEK-293 T (kidney), HuH7 (liver), SH-SY5Y (brain), MCF7 (breast), Huvec (endothelial) and Caco-2 (intestine) was evaluated by RT-qPCR. Concomitantly, expression levels of ACE2 (Angiotensin Converting Enzyme) and TMPRSS2 were assessed through RT-qPCR and western blot. Proteins related to autophagy and mitochondrial metabolism were monitored in uninfected cells to characterize the cellular metabolism of each cell line. The effect of ACE2 overexpression on viral replication in pulmonary cells was also investigated.Our data show that HuH7, Caco-2 and MCF7 presented a higher viral load compared to the other cell lines. The increased susceptibility to SARS-CoV-2 infection seems to be associated not only with the differential levels of proteins intrinsically related to energetic metabolism, such as ATP synthase, citrate synthase, COX and NDUFS2 but also with the considerably higher TMPRSS2 mRNA expression. The two least susceptible cell types, BEAS-2B and A549, showed drastically increased SARS-CoV-2 replication capacity when ACE2 was overexpressed. These modified cell lines are relevant for studying SARS-CoV-2 replication in vitro.Our data not only reinforce that TMPRSS2 expression and cellular energy metabolism are important molecular mechanisms for SARS-CoV-2 infection and replication, but also indicate that HuH7, MCF7 and Caco-2 are suitable models for mechanistic studies of COVID-19. Moreover, pulmonary cells overexpressing ACE2 can be used to understand mechanisms associated with SARS-CoV-2 replication.

Published
2022

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