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Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice

Osteogenesis imperfecta (OI) is a congenital bone dysplasia mainly caused by either defective production or assembly of type I collagen. The skeletal phenotypes especially fractures are often seen in OI adolescents. Studies have found that an increased number of osteoclasts and excessive bone resorp...

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Autores principales: Shao, Chenyi, Liu, Yi, Li, Jiaci, Liu, Ziyun, Zhao, Yuxia, Jing, Yaqing, Lv, Zhe, Fu, Ting, Wang, Zihan, Li, Guang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9415356/
https://www.ncbi.nlm.nih.gov/pubmed/36032950
http://dx.doi.org/10.7717/peerj.13963
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author Shao, Chenyi
Liu, Yi
Li, Jiaci
Liu, Ziyun
Zhao, Yuxia
Jing, Yaqing
Lv, Zhe
Fu, Ting
Wang, Zihan
Li, Guang
author_facet Shao, Chenyi
Liu, Yi
Li, Jiaci
Liu, Ziyun
Zhao, Yuxia
Jing, Yaqing
Lv, Zhe
Fu, Ting
Wang, Zihan
Li, Guang
author_sort Shao, Chenyi
collection PubMed
description Osteogenesis imperfecta (OI) is a congenital bone dysplasia mainly caused by either defective production or assembly of type I collagen. The skeletal phenotypes especially fractures are often seen in OI adolescents. Studies have found that an increased number of osteoclasts and excessive bone resorption existed in collagen-related OI, which has not been well understood. Emerging evidence has suggested that inflammation may be associated with OI. We speculated that the bone marrow (BM) niche had similar inflammatory changes and performed RNA-sequencing (RNA-seq) in BM cells derived from young male mice to analyze the related differentially expressed genes (DEGs) and pathways. Data showed that there were 117 shared DEGs (Q ≤ 0.05, |log(2)FC| ≥ 1) in BM cells isolated from two types of OI murine models that respectively simulate different OI types. Gene Ontology (GO) (Q ≤ 0.05) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) (Q ≤ 0.05) analysis and real-time PCR validation indicated the dysregulated biology process of cellular response to interferon (Ifn) together with upregulated IL-17 signaling, tumor necrosis factor (Tnf) signaling and osteoclast differentiation in OI BM niche. Either defective collagen production or abnormal collagen assembly shared similar alterations in gene profiles and pathways involving inflammation and osteoclast activation. Data presented here not only contributed to understanding of the mechanism of the enhanced bone absorption in the bones of OI, but also provided more evidence to develop potential anti-inflammation therapies.
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spelling pubmed-94153562022-08-27 Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice Shao, Chenyi Liu, Yi Li, Jiaci Liu, Ziyun Zhao, Yuxia Jing, Yaqing Lv, Zhe Fu, Ting Wang, Zihan Li, Guang PeerJ Biochemistry Osteogenesis imperfecta (OI) is a congenital bone dysplasia mainly caused by either defective production or assembly of type I collagen. The skeletal phenotypes especially fractures are often seen in OI adolescents. Studies have found that an increased number of osteoclasts and excessive bone resorption existed in collagen-related OI, which has not been well understood. Emerging evidence has suggested that inflammation may be associated with OI. We speculated that the bone marrow (BM) niche had similar inflammatory changes and performed RNA-sequencing (RNA-seq) in BM cells derived from young male mice to analyze the related differentially expressed genes (DEGs) and pathways. Data showed that there were 117 shared DEGs (Q ≤ 0.05, |log(2)FC| ≥ 1) in BM cells isolated from two types of OI murine models that respectively simulate different OI types. Gene Ontology (GO) (Q ≤ 0.05) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) (Q ≤ 0.05) analysis and real-time PCR validation indicated the dysregulated biology process of cellular response to interferon (Ifn) together with upregulated IL-17 signaling, tumor necrosis factor (Tnf) signaling and osteoclast differentiation in OI BM niche. Either defective collagen production or abnormal collagen assembly shared similar alterations in gene profiles and pathways involving inflammation and osteoclast activation. Data presented here not only contributed to understanding of the mechanism of the enhanced bone absorption in the bones of OI, but also provided more evidence to develop potential anti-inflammation therapies. PeerJ Inc. 2022-08-23 /pmc/articles/PMC9415356/ /pubmed/36032950 http://dx.doi.org/10.7717/peerj.13963 Text en © 2022 Shao et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Biochemistry
Shao, Chenyi
Liu, Yi
Li, Jiaci
Liu, Ziyun
Zhao, Yuxia
Jing, Yaqing
Lv, Zhe
Fu, Ting
Wang, Zihan
Li, Guang
Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title_full Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title_fullStr Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title_full_unstemmed Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title_short Up-regulated IL-17 and Tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
title_sort up-regulated il-17 and tnf signaling in bone marrow cells of young male osteogenesis imperfecta mice
topic Biochemistry
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9415356/
https://www.ncbi.nlm.nih.gov/pubmed/36032950
http://dx.doi.org/10.7717/peerj.13963
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