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TRIM31 promotes apoptosis via TAK1-mediated activation of NF-κB signaling in sepsis-induced myocardial dysfunction
- Source :
- Cell Cycle
- Publication Year :
- 2020
-
Abstract
- Sepsis is a major condition caused by an overwhelming inflammatory response to an infection. Sepsis-induced myocardial dysfunction (SIMD) is a common complication in septic patients and a major predictor of morbidity and mortality. Here, we investigated the role of tripartite motif 31 (TRIM31) protein in sepsis progression in vitro and in vivo. Quantitative real-time PCR and western blot were used to detect the expression levels of relative genes and proteins. Cell proliferation and apoptosis were evaluated to determine cell viability. H&E and IHC staining were performed to examine morphological and pathological changes in mice. ELISA assay was used to detect inflammatory factors. TRIM31 was upregulated in septic patients compared with normal people. TRIM31 depletion reduced LPS-induced apoptosis whereas TRIM31 overexpression-elevated LPS-induced apoptosis. Furthermore, TRIM31 interacted with and ubiquitinated transforming growth factor-β-activated kinase-1 (TAK1), resulting in TAK1 activation and subsequent induction of NF-κB signaling. Of note, Trim31 depletion or blockade by PDTC treatment inhibited LPS-induced apoptosis in vivo. In conclusion, TRIM31 played an important role in SIMD by activating TAK1-mediated NF-κB signaling pathway.
- Subjects :
- 0301 basic medicine
Male
Cell Survival
Ubiquitin-Protein Ligases
Apoptosis
Biology
Cell Line
Sepsis
Tripartite Motif Proteins
03 medical and health sciences
chemistry.chemical_compound
Mice
0302 clinical medicine
Western blot
In vivo
medicine
Animals
Humans
Viability assay
Molecular Biology
Cell Proliferation
Inflammation
medicine.diagnostic_test
Cell Death
Cell growth
Ubiquitin
NF-kappa B
NF-κB
Cell Biology
medicine.disease
MAP Kinase Kinase Kinases
Up-Regulation
Mice, Inbred C57BL
030104 developmental biology
chemistry
030220 oncology & carcinogenesis
Cancer research
Signal transduction
Cardiomyopathies
Developmental Biology
Signal Transduction
Research Paper
Subjects
Details
- ISSN :
- 15514005
- Volume :
- 19
- Issue :
- 20
- Database :
- OpenAIRE
- Journal :
- Cell cycle (Georgetown, Tex.)
- Accession number :
- edsair.doi.dedup.....f888641e37331d350b80129a82e74695