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Regulation of Key Immune-Related Genes in the Heart Following Burn Injury
Immune cascade is one of major factors leading to cardiac dysfunction after burn injury. TLRs are a class of pattern-recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen. The Rat Toll-Like Receptor (T...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9224557/ https://www.ncbi.nlm.nih.gov/pubmed/35743792 http://dx.doi.org/10.3390/jpm12061007 |
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author | Wen, Jake J. Mobli, Keyan Radhakrishnan, Geetha L. Radhakrishnan, Ravi S. |
author_facet | Wen, Jake J. Mobli, Keyan Radhakrishnan, Geetha L. Radhakrishnan, Ravi S. |
author_sort | Wen, Jake J. |
collection | PubMed |
description | Immune cascade is one of major factors leading to cardiac dysfunction after burn injury. TLRs are a class of pattern-recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen. The Rat Toll-Like Receptor (TLR) Signaling Pathway RT² Profiler PCR Array profiles the expression of 84 genes central to TLR-mediated signal transduction and innate immunity, and is a validated tool for identifying differentially expressed genes (DEGs). We employed the PCR array to identify burn-induced cardiac TLR-signaling-related DEGs. A total of 38 up-regulated DEGs and 19 down-regulated DEGs were identified. Network analysis determined that all DEGS had 10 clusters, while up-regulated DEGs had 6 clusters and down-regulated DEGs had 5 clusters. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were involved in TLR signaling, the RIG-I-Like receptor signaling pathway, the IL-17 signaling pathway, and the NFkB signaling pathway. Function analysis indicated that DEGs were associated with Toll-like receptor 2 binding, Lipopeptide binding, Toll-like receptor binding, and NAD(P)+ nucleosidase activity. The validation of 18 up-regulated DEGs (≥10-fold change) and 6 down-regulated DEGs (≤5-fold change) demonstrated that the PCR array is a trusted method for identifying DEGs. The analysis of validated DEG-derived protein–protein interaction networks will guide our future investigations. In summary, this study not only identified the TLR-signaling-pathway-related DEGs after burn injury, but also confirmed that the burn-induced cardiac cytokine cascade plays an important role in burn-induced heart dysfunction. The results will provide the novel therapeutic targets to protect the heart after burn injury. |
format | Online Article Text |
id | pubmed-9224557 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-92245572022-06-24 Regulation of Key Immune-Related Genes in the Heart Following Burn Injury Wen, Jake J. Mobli, Keyan Radhakrishnan, Geetha L. Radhakrishnan, Ravi S. J Pers Med Article Immune cascade is one of major factors leading to cardiac dysfunction after burn injury. TLRs are a class of pattern-recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen. The Rat Toll-Like Receptor (TLR) Signaling Pathway RT² Profiler PCR Array profiles the expression of 84 genes central to TLR-mediated signal transduction and innate immunity, and is a validated tool for identifying differentially expressed genes (DEGs). We employed the PCR array to identify burn-induced cardiac TLR-signaling-related DEGs. A total of 38 up-regulated DEGs and 19 down-regulated DEGs were identified. Network analysis determined that all DEGS had 10 clusters, while up-regulated DEGs had 6 clusters and down-regulated DEGs had 5 clusters. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were involved in TLR signaling, the RIG-I-Like receptor signaling pathway, the IL-17 signaling pathway, and the NFkB signaling pathway. Function analysis indicated that DEGs were associated with Toll-like receptor 2 binding, Lipopeptide binding, Toll-like receptor binding, and NAD(P)+ nucleosidase activity. The validation of 18 up-regulated DEGs (≥10-fold change) and 6 down-regulated DEGs (≤5-fold change) demonstrated that the PCR array is a trusted method for identifying DEGs. The analysis of validated DEG-derived protein–protein interaction networks will guide our future investigations. In summary, this study not only identified the TLR-signaling-pathway-related DEGs after burn injury, but also confirmed that the burn-induced cardiac cytokine cascade plays an important role in burn-induced heart dysfunction. The results will provide the novel therapeutic targets to protect the heart after burn injury. MDPI 2022-06-20 /pmc/articles/PMC9224557/ /pubmed/35743792 http://dx.doi.org/10.3390/jpm12061007 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Wen, Jake J. Mobli, Keyan Radhakrishnan, Geetha L. Radhakrishnan, Ravi S. Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title | Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title_full | Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title_fullStr | Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title_full_unstemmed | Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title_short | Regulation of Key Immune-Related Genes in the Heart Following Burn Injury |
title_sort | regulation of key immune-related genes in the heart following burn injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9224557/ https://www.ncbi.nlm.nih.gov/pubmed/35743792 http://dx.doi.org/10.3390/jpm12061007 |
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