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TACSTD2 upregulation is an early reaction to lung infection
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....
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9185727/ https://www.ncbi.nlm.nih.gov/pubmed/35688908 http://dx.doi.org/10.1038/s41598-022-13637-9 |
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author | Lenárt, Sára Lenárt, Peter Knopfová, Lucia Kotasová, Hana Pelková, Vendula Sedláková, Veronika Vacek, Ondřej Pokludová, Jana Čan, Vladimír Šmarda, Jan Souček, Karel Hampl, Aleš Beneš, Petr |
author_facet | Lenárt, Sára Lenárt, Peter Knopfová, Lucia Kotasová, Hana Pelková, Vendula Sedláková, Veronika Vacek, Ondřej Pokludová, Jana Čan, Vladimír Šmarda, Jan Souček, Karel Hampl, Aleš Beneš, Petr |
author_sort | Lenárt, Sára |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9185727 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-91857272022-06-10 TACSTD2 upregulation is an early reaction to lung infection Lenárt, Sára Lenárt, Peter Knopfová, Lucia Kotasová, Hana Pelková, Vendula Sedláková, Veronika Vacek, Ondřej Pokludová, Jana Čan, Vladimír Šmarda, Jan Souček, Karel Hampl, Aleš Beneš, Petr Sci Rep Article 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. Nature Publishing Group UK 2022-06-10 /pmc/articles/PMC9185727/ /pubmed/35688908 http://dx.doi.org/10.1038/s41598-022-13637-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Lenárt, Sára Lenárt, Peter Knopfová, Lucia Kotasová, Hana Pelková, Vendula Sedláková, Veronika Vacek, Ondřej Pokludová, Jana Čan, Vladimír Šmarda, Jan Souček, Karel Hampl, Aleš Beneš, Petr TACSTD2 upregulation is an early reaction to lung infection |
title | TACSTD2 upregulation is an early reaction to lung infection |
title_full | TACSTD2 upregulation is an early reaction to lung infection |
title_fullStr | TACSTD2 upregulation is an early reaction to lung infection |
title_full_unstemmed | TACSTD2 upregulation is an early reaction to lung infection |
title_short | TACSTD2 upregulation is an early reaction to lung infection |
title_sort | tacstd2 upregulation is an early reaction to lung infection |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9185727/ https://www.ncbi.nlm.nih.gov/pubmed/35688908 http://dx.doi.org/10.1038/s41598-022-13637-9 |
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