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TACSTD2 upregulation is an early reaction to lung infection
S. Lenárt, P. Lenárt, L. Knopfová, H. Kotasová, V. Pelková, V. Sedláková, O. Vacek, J. Pokludová, V. Čan, J. Šmarda, K. Souček, A. Hampl, P. Beneš
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články
Grantová podpora
21-11585S
Grantová Agentura České Republiky
18-00145S
Grantová Agentura České Republiky
MUNI/A/1689/2020
Masarykova Univerzita
MUNI/A/1522/2020
Masarykova Univerzita
NV18-07-00073
Ministerstvo Zdravotnictví Ceské Republiky
CZ.02.1.01/0.0/16_019/0000868
European Regional Development Fund
NLK
Directory of Open Access Journals
od 2011
Free Medical Journals
od 2011
Nature Open Access
od 2011-12-01
PubMed Central
od 2011
Europe PubMed Central
od 2011
ProQuest Central
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Open Access Digital Library
od 2011-01-01
Health & Medicine (ProQuest)
od 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2011
Springer Nature OA/Free Journals
od 2011-12-01
- MeSH
- antigeny nádorové * metabolismus MeSH
- epitelové buňky metabolismus MeSH
- molekuly buněčné adheze * metabolismus MeSH
- plíce metabolismus MeSH
- upregulace MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
TACSTD2 encodes a transmembrane glycoprotein Trop2 commonly overexpressed in carcinomas. While the Trop2 protein was discovered already in 1981 and first antibody-drug conjugate targeting Trop2 were recently approved for cancer therapy, the physiological role of Trop2 is still not fully understood. In this article, we show that TACSTD2/Trop2 expression is evolutionarily conserved in lungs of various vertebrates. By analysis of publicly available transcriptomic data we demonstrate that TACSTD2 level consistently increases in lungs infected with miscellaneous, but mainly viral pathogens. Single cell and subpopulation based transcriptomic data revealed that the major source of TACSTD2 transcript are lung epithelial cells and their progenitors and that TACSTD2 is induced directly in lung epithelial cells following infection. Increase in TACSTD2 expression may represent a mechanism to maintain/restore epithelial barrier function and contribute to regeneration process in infected/damaged lungs.
Department of Histology and Embryology Faculty of Medicine Masaryk University Brno Czech Republic
Department of Surgery University Hospital Brno Brno Czech Republic
Institute of Cell Biology University of Bern Bern Switzerland
International Clinical Research Center St Anne's University Hospital Brno Czech Republic
Citace poskytuje Crossref.org
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- $a TACSTD2 encodes a transmembrane glycoprotein Trop2 commonly overexpressed in carcinomas. While the Trop2 protein was discovered already in 1981 and first antibody-drug conjugate targeting Trop2 were recently approved for cancer therapy, the physiological role of Trop2 is still not fully understood. In this article, we show that TACSTD2/Trop2 expression is evolutionarily conserved in lungs of various vertebrates. By analysis of publicly available transcriptomic data we demonstrate that TACSTD2 level consistently increases in lungs infected with miscellaneous, but mainly viral pathogens. Single cell and subpopulation based transcriptomic data revealed that the major source of TACSTD2 transcript are lung epithelial cells and their progenitors and that TACSTD2 is induced directly in lung epithelial cells following infection. Increase in TACSTD2 expression may represent a mechanism to maintain/restore epithelial barrier function and contribute to regeneration process in infected/damaged lungs.
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