Transcriptomic study of lipopolysaccharide‑induced sepsis damage in a mouse heart model
- Cunrong Chen
- Junting Weng
- Dexiang Fang
- Jianfei Chen
- Min Chen
Affiliations: Department of Critical Care Medicine, Union Hospital Affiliated to Fujian Medical University, Fuzhou, Fujian 350000, P.R. China, Department of Critical Care Medicine, Affiliated Hospital of Putian University, Putian, Fujian 351100, P.R. China
- Published online on: July 31, 2020 https://doi.org/10.3892/etm.2020.9086
Copyright: © Chen
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Sepsis is an emergency systemic illness caused by pathogen infection and the combined result of the underactivity and overactivity of a patient's own immune system. However, the molecular mechanism of this illness remains largely unknown. Lipopolysaccharide (LPS) was injected to establish a sepsis model, and heart tissue was used to analyze transcriptome changes in mice. LPS injection was used to develop a sepsis model, which resulted in cardiac tissue rearrangement and inflammatory response activation. An RNA‑sequencing‑based transcriptome assay using mouse heart tissue with or without LPS injection showed that 3,326 and 1,769 genes were upregulated and downregulated, respectively (>2‑fold changes; P<0.05). Furthermore, these differentially expressed genes were classified into 20 pathways, including ‘Wnt signaling pathway’, ‘VEGF signaling pathway’ and ‘TGF‑β signaling pathway’, and these altered genes were enriched in 41 Gene Ontology terms. The application of Wnt3a inhibited the activation of the LPS‑induced inflammatory response and activated Wnt signaling, as well as protecting against LPS‑mediated cardiac tissue damage in mice. In contrast, inhibition of Wnt signaling by injection of its inhibitor IWR induced plasminogen activator inhibitor‑1 expression and resulted in cardiac structure derangement, which was similar to the symptoms caused by injection of LPS, suggesting that LPS‑induced damage to heart tissue may be via inhibition of Wnt signaling. The present analyses showed that Wnt signaling serves a pivotal role in sepsis development and may improve our understanding of the molecular basis underlying sepsis.