The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages

Abstract Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, el...

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Autores principales:	Shotaro Eto, Hideyuki Yanai, Sho Hangai, Daiki Kato, Ryohei Nishimura, Takayuki Nakagawa
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/22d60bea34a74a2f9e372f6b97c7a09b
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spelling	oai:doaj.org-article:22d60bea34a74a2f9e372f6b97c7a09b2021-12-02T13:39:34ZThe impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages10.1038/s41598-021-87979-12045-2322https://doaj.org/article/22d60bea34a74a2f9e372f6b97c7a09b2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87979-1https://doaj.org/toc/2045-2322Abstract Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, elucidating the role of damage-associated molecules in inducing sterile immune responses is crucial. In this study, we show that prostaglandin E2 (PGE2) is produced in the supernatants from several types of canine necrotic tumor cell lines. Inhibition of PGE2 production by indomethacin, a potent inhibitor of cyclooxygenase (COX) enzymes, induces the expression of tumor necrosis factor (Tnf) mRNA in the necrotic tumor cell supernatants. These results comply with the previous observations reported in mouse cell lines. Furthermore, comprehensive ribonucleic acid-sequencing (RNA-seq) analysis revealed that three categories of genes were induced by the damage-associated molecules: (i) a group of PGE2-inducible genes, (ii) genes that promote inflammation and are suppressed by PGE2, and (iii) a group of genes not suppressed by PGE2. Collectively, our findings reveal the hitherto unknown immune regulatory system by PGE2 and damage-associated molecules, which may have clinical implications in inflammation and cancer.Shotaro EtoHideyuki YanaiSho HangaiDaiki KatoRyohei NishimuraTakayuki NakagawaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shotaro Eto Hideyuki Yanai Sho Hangai Daiki Kato Ryohei Nishimura Takayuki Nakagawa The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
description	Abstract Dying or damaged cells that are not completely eradicated by the immune system release their intracellular components in the extracellular space. Aberrant exposure of the damage-associated molecules to the immune system is often associated with inflammation and cancer pathogenesis. Thus, elucidating the role of damage-associated molecules in inducing sterile immune responses is crucial. In this study, we show that prostaglandin E2 (PGE2) is produced in the supernatants from several types of canine necrotic tumor cell lines. Inhibition of PGE2 production by indomethacin, a potent inhibitor of cyclooxygenase (COX) enzymes, induces the expression of tumor necrosis factor (Tnf) mRNA in the necrotic tumor cell supernatants. These results comply with the previous observations reported in mouse cell lines. Furthermore, comprehensive ribonucleic acid-sequencing (RNA-seq) analysis revealed that three categories of genes were induced by the damage-associated molecules: (i) a group of PGE2-inducible genes, (ii) genes that promote inflammation and are suppressed by PGE2, and (iii) a group of genes not suppressed by PGE2. Collectively, our findings reveal the hitherto unknown immune regulatory system by PGE2 and damage-associated molecules, which may have clinical implications in inflammation and cancer.
format	article
author	Shotaro Eto Hideyuki Yanai Sho Hangai Daiki Kato Ryohei Nishimura Takayuki Nakagawa
author_facet	Shotaro Eto Hideyuki Yanai Sho Hangai Daiki Kato Ryohei Nishimura Takayuki Nakagawa
author_sort	Shotaro Eto
title	The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
title_short	The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
title_full	The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
title_fullStr	The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
title_full_unstemmed	The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
title_sort	impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/22d60bea34a74a2f9e372f6b97c7a09b
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The impact of damage-associated molecules released from canine tumor cells on gene expression in macrophages

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