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CD14 Involvement in Third-degree Skin Burn-induced Myocardial Injury via the MAPK Signaling Pathway
Zhensen Zhu1, Ben Zou1, Songying Gao1
1The Department of Plastic and Burn Surgery, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Cell Biochemistry and Biophysics
|July 23, 2021
Summary
Third-degree burns cause myocardial injury by inducing apoptosis via the mitogen-activated protein kinase (MAPK) pathway. Interfering with CD14 expression reversed these burn-induced effects, highlighting CD14
Area of Science:
- Biomedical research
- Molecular biology
- Cardiovascular pathology
Background:
- Third-degree burns can lead to myocardial injury.
- Understanding the molecular mechanisms of burn-induced myocardial injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the genes and signaling pathways involved in burn-induced myocardial injury.
- To identify key molecular players, such as CD14, in this process.
Main Methods:
- Utilized rat models of third-degree burn.
- Employed hematoxylin & eosin staining, TUNEL staining, and ELISA for histopathological and apoptosis analysis.
- Conducted next-generation sequencing (NGS) to identify differentially expressed mRNAs.
- Validated key genes using quantitative reverse transcription-polymerase chain reaction (RT-qPCR).
- Used H9C2 cells and small interfering RNAs (siRNAs) against CD14 to verify its role.
Main Results:
- Third-degree burns induced significant myocardial structural damage, apoptosis, and elevated cardiac injury markers in rats.
- NGS identified 416 upregulated and 285 downregulated mRNAs in myocardial tissue post-burn.
- Differentially expressed genes were primarily enriched in phosphatidylinositol 3-kinase/Akt, mitogen-activated protein kinase (MAPK), and tumor necrosis factor signaling pathways.
- Burn serum decreased H9C2 cell viability and activated the MAPK pathway (ERK, p38, JNK), increasing cleaved caspase-3 and decreasing Bcl2.
- CD14 was significantly differentially expressed, and interfering with its expression reversed the effects of burn serum on MAPK signaling and apoptosis.
Conclusions:
- Third-degree burns induce myocardial injury in rats through mechanisms involving apoptosis and the MAPK signaling pathway.
- CD14 plays a significant role in burn-induced myocardial injury by modulating MAPK pathway activation and subsequent apoptosis.
- Targeting CD14 may represent a potential therapeutic strategy for mitigating burn-induced myocardial damage.
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