FAM46C inhibits lipopolysaccharides-induced myocardial dysfunction via downregulating cellular adhesion molecules and inhibiting apoptosis

Sepsis is a syndrome of inflammatory response induced by infection. Cellular adhesion molecules may involve in sepsis-induced myocardial dysfunction (SIMD) which is a major predictor of morbidity and mortality of sepsis. Here we studied the role of FAM46C in AC16 cells and c57 mice with lipopolysacc...

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Bibliographic Details
Published in:Life sciences (1973) 2019-07, Vol.229, p.1-12
Main Authors: Tan, Jiaying, Sun, Tao, Shen, Jun, Zhu, Huigeng, Gong, Ye, Zhu, Hechen, Wu, Gang
Format: Article
Language:English
Subjects:
Adhesion
Apoptosis
Cell adhesion molecules
Cell proliferation
FAM46C
Gene expression
Immune system
Inflammation
Inflammatory response
Inhibition
Lipopolysaccharides
MAP kinase
Morbidity
Proteins
Sepsis
Signal transduction
SIMD
TLR4
TLR4 protein
Toll-like receptors
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Summary:Sepsis is a syndrome of inflammatory response induced by infection. Cellular adhesion molecules may involve in sepsis-induced myocardial dysfunction (SIMD) which is a major predictor of morbidity and mortality of sepsis. Here we studied the role of FAM46C in AC16 cells and c57 mice with lipopolysaccharides (LPS) treatment. Real-time PCR and western blot were used to detect the expression level of relative genes and protein. Cell proliferation and apoptosis were evaluated. Interestingly, negative correlation between Toll-like receptor 4 (TLR4) and FAM46C in sepsis was observed. The overexpression of FAM46C reduced the apoptosis induced by LPS in AC16 cells. Inhibition of apoptosis contributed by FAM46C was mediated by adhesion molecule via blocking p38 and ERK/MAPK signaling pathway. Moreover, overexpression of Fam46c and inhibition of TLR4 by TAK-242 could attenuate apoptosis induced by LPS in vivo. FAM46C played an important role in SIMD via inhibiting LPS-induced myocardial dysfunction by downregulating cellular adhesion molecules and inhibiting apoptosis. It was the first time to explore the role of FAM46C in SIMD in this study.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2019.03.048