2022
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. Journal Article
In: Scientific reports, vol. 12, no. 1, pp. 9583, 2022, ISSN: 2045-2322, (Place: England).
Abstract | Links | BibTeX | Tags: *Antigens, *Cell Adhesion Molecules/metabolism, Animals, Epithelial Cells/metabolism, Lung/metabolism, Neoplasm/metabolism, Up-Regulation
@article{lenart_tacstd2_2022,
title = {TACSTD2 upregulation is an early reaction to lung infection.},
author = {Sára Lenárt and Peter Lenárt and Lucia Knopfová and Hana Kotasová and Vendula Pelková and Veronika Sedláková and Ondřej Vacek and Jana Pokludová and Vladimír Čan and Jan Šmarda and Karel Souček and Aleš Hampl and Petr Beneš},
doi = {10.1038/s41598-022-13637-9},
issn = {2045-2322},
year = {2022},
date = {2022-06-01},
journal = {Scientific reports},
volume = {12},
number = {1},
pages = {9583},
abstract = {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.},
note = {Place: England},
keywords = {*Antigens, *Cell Adhesion Molecules/metabolism, Animals, Epithelial Cells/metabolism, Lung/metabolism, Neoplasm/metabolism, Up-Regulation},
pubstate = {published},
tppubtype = {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.