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Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice

To find potential biomarkers based on miRNA and their potential targets in splenic monocytes in burn‐injured mice. Male Balb/c mice were subjected to sham or scalding injury of 15% total body surface area. Spenic CD11b+ monocytes were purified with magnetic beads. The monocytes were cultured in the...

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Autores principales: Liu, Hong‐sheng, Li, Lun‐chao, Wang, Man, Liu, Dong‐sheng, Su, Qin, Zhang, Qing‐Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10681402/
https://www.ncbi.nlm.nih.gov/pubmed/37386845
http://dx.doi.org/10.1111/iwj.14288
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author Liu, Hong‐sheng
Li, Lun‐chao
Wang, Man
Liu, Dong‐sheng
Su, Qin
Zhang, Qing‐Hong
author_facet Liu, Hong‐sheng
Li, Lun‐chao
Wang, Man
Liu, Dong‐sheng
Su, Qin
Zhang, Qing‐Hong
author_sort Liu, Hong‐sheng
collection PubMed
description To find potential biomarkers based on miRNA and their potential targets in splenic monocytes in burn‐injured mice. Male Balb/c mice were subjected to sham or scalding injury of 15% total body surface area. Spenic CD11b+ monocytes were purified with magnetic beads. The monocytes were cultured in the presence of lipopolysaccharide. The proliferation of monocytes was detected by MTT assay, and the cytokines in the supernatant were examined by enzyme linked immunosorbent assay. The purified monocytes were also under total RNA extraction. The differential monocytic miRNAs expression between the sham and burn‐injured mice was analysed by miRNA microarray. The activity of monocytes was comparable between the two groups (p > 0.05). However, monocytes from burn‐injured mice secreted higher levels of tumour necrosis factor (TNF)‐α and transforming growth factor‐β, but lower level of monocyte chemoattratctant protein‐1. A total of 54 miRNAs were differentially expressed in monocytes from burn relative to sham‐injured mice (fold >3). Further quantitative reverse transcription polymerase chain reaction confirmed that the expression of miR‐146a was significantly down‐regulated, while miR‐3091‐6p was up‐regulated after burn injury. Using the combination of Miranda and TargetScan softwares, we found that mir‐146a may regulate 180 potential target genes including TNF receptor related factor 6 (TRAF6), interleukin‐1 receptor related kinase 1 (IRAK1) and CD28. Mir‐3091‐6p may regulate 39 potential targets, including SOCS7 (cytokine signal transduction inhibitor 7) and ARRB2 (arrestin, β 2). The miRNAs expressed by monocytes after burn injury may be involved in the regulation of innate immune response in burn injury.
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spelling pubmed-106814022023-06-29 Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice Liu, Hong‐sheng Li, Lun‐chao Wang, Man Liu, Dong‐sheng Su, Qin Zhang, Qing‐Hong Int Wound J Original Articles To find potential biomarkers based on miRNA and their potential targets in splenic monocytes in burn‐injured mice. Male Balb/c mice were subjected to sham or scalding injury of 15% total body surface area. Spenic CD11b+ monocytes were purified with magnetic beads. The monocytes were cultured in the presence of lipopolysaccharide. The proliferation of monocytes was detected by MTT assay, and the cytokines in the supernatant were examined by enzyme linked immunosorbent assay. The purified monocytes were also under total RNA extraction. The differential monocytic miRNAs expression between the sham and burn‐injured mice was analysed by miRNA microarray. The activity of monocytes was comparable between the two groups (p > 0.05). However, monocytes from burn‐injured mice secreted higher levels of tumour necrosis factor (TNF)‐α and transforming growth factor‐β, but lower level of monocyte chemoattratctant protein‐1. A total of 54 miRNAs were differentially expressed in monocytes from burn relative to sham‐injured mice (fold >3). Further quantitative reverse transcription polymerase chain reaction confirmed that the expression of miR‐146a was significantly down‐regulated, while miR‐3091‐6p was up‐regulated after burn injury. Using the combination of Miranda and TargetScan softwares, we found that mir‐146a may regulate 180 potential target genes including TNF receptor related factor 6 (TRAF6), interleukin‐1 receptor related kinase 1 (IRAK1) and CD28. Mir‐3091‐6p may regulate 39 potential targets, including SOCS7 (cytokine signal transduction inhibitor 7) and ARRB2 (arrestin, β 2). The miRNAs expressed by monocytes after burn injury may be involved in the regulation of innate immune response in burn injury. Blackwell Publishing Ltd 2023-06-29 /pmc/articles/PMC10681402/ /pubmed/37386845 http://dx.doi.org/10.1111/iwj.14288 Text en © 2023 The Authors. International Wound Journal published by Medicalhelplines.com Inc and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Liu, Hong‐sheng
Li, Lun‐chao
Wang, Man
Liu, Dong‐sheng
Su, Qin
Zhang, Qing‐Hong
Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title_full Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title_fullStr Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title_full_unstemmed Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title_short Differentiated expressed miRNAs in splenic monocyte induced by burn injury in mice
title_sort differentiated expressed mirnas in splenic monocyte induced by burn injury in mice
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10681402/
https://www.ncbi.nlm.nih.gov/pubmed/37386845
http://dx.doi.org/10.1111/iwj.14288
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