CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury

Jia-Xin Shi,1 Jia-Shu Li,1 Rong Hu,1 Xiao-Min Li,2 Hong Wang3 1Department of Respiratory Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing Medical University, Clinical Medical Schoo...

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Autores principales:	Shi JX, Li JS, Hu R, Li XM, Wang H
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2016
Materias:	CAF1 knockout mice acute lung injury IL-8 ICAM-1 Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/20e26b637aa74619b0a337a414f7c8d7
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spelling	oai:doaj.org-article:20e26b637aa74619b0a337a414f7c8d72021-12-02T00:31:40ZCAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury1178-7031https://doaj.org/article/20e26b637aa74619b0a337a414f7c8d72016-06-01T00:00:00Zhttps://www.dovepress.com/caf1-knockout-mice-are-more-susceptive-to-lipopolysaccharide-induced-a-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Jia-Xin Shi,1 Jia-Shu Li,1 Rong Hu,1 Xiao-Min Li,2 Hong Wang3 1Department of Respiratory Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing Medical University, Clinical Medical School of Jiangsu University, Lianyungang, 2Department of Critical Care Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing Medical University, Clinical Medical School of Jiangsu University, Lianyungang, 3Department of Respiratory Medicine, Jiangsu Province Hospital, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China Abstract: The carbon catabolite repressor protein 4 (CCR4)–negative on TATA (NOT) complex includes multiple subunits and is conserved in the eukaryotic cells. The CCR4–NOT complex can regulate gene expression at different levels. Two subunits of the CCR4–NOT complex, CCR4 and CCR4-associated factor 1 (CAF1), possess deadenylase activity. In yeast, the deadenylase activity is mainly provided by the CCR4 subunit; however, the deadenylase activity is provided by both CCR4 and CAF1 in other eukaryotes. A previous study reported that CAF1 but not CCR4 is required for the decay of a reporter mRNA with AU-rich elements. Our previous study showed that CAF1 is involved in the regulation of intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) expression. Both ICAM-1 and IL-8 play crucial roles in acute lung injury. In the present study, we examined the effects of CAF1 deficiency on IL-8 and ICAM-1 expression and acute lung injury in mice. Here we showed that there were no differences between the wild-type and CAF1-knockout mice on phenotypes. The lung histology and protein and mRNA levels of IL-8 and ICAM-1 in unstimulated wild-type mice were comparable to those in unstimulated CAF1-knockout mice. However, lipopolysaccharide stimulation led to more severe lung histological injury and greatly higher IL-8 and ICAM-1 expression in CAF1-knockout mice compared to the wild-type mice. These results, together with our previous study, suggest that CAF1 is involved in the regulation of lipopolysaccharide-stimulated IL-8 and ICAM-1 expression in vivo and affects the progression of acute lung injury. Keywords: CAF1, knockout, mice, acute lung injury, IL-8, ICAM-1Shi JXLi JSHu RLi XMWang HDove Medical PressarticleCAF1knockoutmiceacute lung injuryIL-8ICAM-1PathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol 2016, Iss Issue 1, Pp 115-121 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	CAF1 knockout mice acute lung injury IL-8 ICAM-1 Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	CAF1 knockout mice acute lung injury IL-8 ICAM-1 Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Shi JX Li JS Hu R Li XM Wang H CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
description	Jia-Xin Shi,1 Jia-Shu Li,1 Rong Hu,1 Xiao-Min Li,2 Hong Wang3 1Department of Respiratory Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing Medical University, Clinical Medical School of Jiangsu University, Lianyungang, 2Department of Critical Care Medicine, Lianyungang First People’s Hospital, Affiliated Hospital of Xuzhou Medical University, Affiliated Hospital of the Clinical Medical School of Nanjing Medical University, Clinical Medical School of Jiangsu University, Lianyungang, 3Department of Respiratory Medicine, Jiangsu Province Hospital, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China Abstract: The carbon catabolite repressor protein 4 (CCR4)–negative on TATA (NOT) complex includes multiple subunits and is conserved in the eukaryotic cells. The CCR4–NOT complex can regulate gene expression at different levels. Two subunits of the CCR4–NOT complex, CCR4 and CCR4-associated factor 1 (CAF1), possess deadenylase activity. In yeast, the deadenylase activity is mainly provided by the CCR4 subunit; however, the deadenylase activity is provided by both CCR4 and CAF1 in other eukaryotes. A previous study reported that CAF1 but not CCR4 is required for the decay of a reporter mRNA with AU-rich elements. Our previous study showed that CAF1 is involved in the regulation of intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) expression. Both ICAM-1 and IL-8 play crucial roles in acute lung injury. In the present study, we examined the effects of CAF1 deficiency on IL-8 and ICAM-1 expression and acute lung injury in mice. Here we showed that there were no differences between the wild-type and CAF1-knockout mice on phenotypes. The lung histology and protein and mRNA levels of IL-8 and ICAM-1 in unstimulated wild-type mice were comparable to those in unstimulated CAF1-knockout mice. However, lipopolysaccharide stimulation led to more severe lung histological injury and greatly higher IL-8 and ICAM-1 expression in CAF1-knockout mice compared to the wild-type mice. These results, together with our previous study, suggest that CAF1 is involved in the regulation of lipopolysaccharide-stimulated IL-8 and ICAM-1 expression in vivo and affects the progression of acute lung injury. Keywords: CAF1, knockout, mice, acute lung injury, IL-8, ICAM-1
format	article
author	Shi JX Li JS Hu R Li XM Wang H
author_facet	Shi JX Li JS Hu R Li XM Wang H
author_sort	Shi JX
title	CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
title_short	CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
title_full	CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
title_fullStr	CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
title_full_unstemmed	CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
title_sort	caf1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury
publisher	Dove Medical Press
publishDate	2016
url	https://doaj.org/article/20e26b637aa74619b0a337a414f7c8d7
work_keys_str_mv	AT shijx caf1knockoutmicearemoresusceptivetolipopolysaccharideinducedacutelunginjury AT lijs caf1knockoutmicearemoresusceptivetolipopolysaccharideinducedacutelunginjury AT hur caf1knockoutmicearemoresusceptivetolipopolysaccharideinducedacutelunginjury AT lixm caf1knockoutmicearemoresusceptivetolipopolysaccharideinducedacutelunginjury AT wangh caf1knockoutmicearemoresusceptivetolipopolysaccharideinducedacutelunginjury
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CAF1-knockout mice are more susceptive to lipopolysaccharide-induced acute lung injury

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