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No evidence that androgen regulation of pulmonary TMPRSS2 explains sex-discordant COVID-19 outcomes

Mehdi Baratchian, Jeffrey McManus, Mike Berk, Fumihiko Nakamura, Serpil Erzurum, Sanjay Mukhopadhyay, Judy Drazba, John Peterson, Ben Gaston, View ORCID ProfileNima Sharifi
doi: https://doi.org/10.1101/2020.04.21.051201
Mehdi Baratchian
1Genitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic
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Jeffrey McManus
1Genitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic
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Mike Berk
1Genitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic
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Fumihiko Nakamura
1Genitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic
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Serpil Erzurum
2Department of Pathobiology, Lerner Research Institute, Cleveland Clinic
3Respiratory Institute, Cleveland Clinic
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Sanjay Mukhopadhyay
4Pathology and Laboratory Medicine Institute, Cleveland Clinic
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Judy Drazba
5Imaging Core, Lerner Research Institute, Cleveland Clinic
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John Peterson
5Imaging Core, Lerner Research Institute, Cleveland Clinic
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Ben Gaston
6Herman Wells Center for Pediatric Research, Indiana University School of Medicine
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Nima Sharifi
1Genitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic
7Department of Urology, Glickman Urological and Kidney Institute, Cleveland Clinic
8Department of Hematology and Oncology, Taussig Cancer Institute, Cleveland Clinic
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  • ORCID record for Nima Sharifi
  • For correspondence: sharifn@ccf.org
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Abstract

The recent emergence of SARS-CoV-2 and the subsequent COVID-19 pandemic have posed a public health crisis. Higher morbidity and mortality of men with COVID-19 may be explained by androgen-driven mechanisms. One such proposed mechanism is androgen regulation of pulmonary TMPRSS2, the host co-receptor for SARS-CoV-2. We find no evidence for increased TMPRSS2 mRNA expression in the lungs of males compared to females in humans or mice. Furthermore, in male mice, treatment with the androgen receptor antagonist enzalutamide does not decrease pulmonary TMPRSS2 expression. Nevertheless, regardless of sex, smoking significantly increases the expression of TMPRSS2, which reverts back to never-smoker levels in former smokers. Finally, we show that in mouse models, despite equivalent AR transcript levels, males express markedly higher amounts of AR protein. If a similar sex-specific regulation of AR protein occurs in human lung, androgens could play important roles in clinical outcome of COVID-19 through mechanisms other than TMPRSS2 regulation.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted April 21, 2020.
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No evidence that androgen regulation of pulmonary TMPRSS2 explains sex-discordant COVID-19 outcomes
Mehdi Baratchian, Jeffrey McManus, Mike Berk, Fumihiko Nakamura, Serpil Erzurum, Sanjay Mukhopadhyay, Judy Drazba, John Peterson, Ben Gaston, Nima Sharifi
bioRxiv 2020.04.21.051201; doi: https://doi.org/10.1101/2020.04.21.051201
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No evidence that androgen regulation of pulmonary TMPRSS2 explains sex-discordant COVID-19 outcomes
Mehdi Baratchian, Jeffrey McManus, Mike Berk, Fumihiko Nakamura, Serpil Erzurum, Sanjay Mukhopadhyay, Judy Drazba, John Peterson, Ben Gaston, Nima Sharifi
bioRxiv 2020.04.21.051201; doi: https://doi.org/10.1101/2020.04.21.051201

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