Key result
TIFA knockdown inhibited inflammatory cell infiltration, pro-inflammatory mediator production, NF-κB activation, and cardiac remodelling post-AMI in a mouse model.
Why the study?
Post-AMI cardiac remodelling is driven by excess inflammatory responses, and TIFA acts as an NF-κB activator, but its expression and underlying mechanism in AMI were unclear.
Does TIFA knockdown reduce inflammatory cell infiltration and cardiac remodelling in an AMI mouse model?
Does TIFA knockdown reduce inflammatory cell infiltration and cardiac remodelling in an AMI mouse model?
TIFA inhibition ameliorates cardiac remodelling after acute myocardial infarction partly through inactivation of NF-κB in a preclinical model.
OBJECTIVES: Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. Post-AMI cardiac remodelling is closely related to the prognosis of AMI. The excess inflammatory responses could promote cardiac remodelling. Tumour necrosis factor receptor-associated factor-interacting protein with forkhead-associated domain (TIFA) has been identified as a nuclear factor (NF)-κB activator, which plays a key role in the activation of the NF-κB signalling pathway. The goal of this research was to investigate the expression and the underlying mechanism of TIFA in an AMI mouse model. METHODS: The AMI mouse model was induced by ligation of the left coronary artery. TIFA and NF-κB knockdown were established by lentivirus transduction. The expression levels of associated proteins were analysed by a western blot or an enzyme-linked immunosorbent assay. Histological characteristics were evaluated by haematoxylin-eosin staining. RESULTS: The TIFA level was elevated in our AMI mouse model. The production of interleukin-1β and tumour necrosis factor-α increased markedly in the mice with AMI. TIFA knockdown inhibited the infiltration of inflammatory cells, production of pro-inflammatory mediators (interleukin-1β and tumour necrosis factor-α), NF-κB activation and cardiac remodelling (matrix metallopeptidase 9) post-AMI. In addition, NF-κB knockdown could also alleviate cardiac remodelling after AMI. CONCLUSIONS: The preceding results indicated that TIFA inhibition could ameliorate cardiac remodelling after AMI partly through inactivation of NF-κB. This study provides insights into further research of cardiac remodelling and AMI from bench to clinic.
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Jiang et al. (2020) studied Acute myocardial infarction. TIFA knockdown vs. Control (AMI without knockdown) was evaluated on Inflammatory cell infiltration, pro-inflammatory mediators, NF-κB activation, and cardiac remodelling. TIFA knockdown inhibited inflammatory cell infiltration, pro-inflammatory mediator production, NF-κB activation, and cardiac remodelling post-AMI in a mouse model.
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