Key result
CRP increases NCX1 expression and intracellular calcium in cardiomyocytes via the NF-κB pathway.
Why the study?
C-reactive protein is associated with cardiac arrhythmia and cardiac remodeling, but the underlying mechanisms remain unclear.
CRP upregulates NCX1 expression and increases intracellular calcium concentration in cardiomyocytes via the NF-κB pathway, providing a potential cellular mechanism for CRP-associated arrhythmias.
Numerous previous studies have found that C-reactive protein (CRP) is associated with cardiac arrhythmia and cardiac remodeling. However, the underlying mechanisms of this association remain unclear. Sodium-calcium exchanger 1 (NCX1) serves an important role in the regulation of intracellular calcium concentration, which is closely related with cardiac arrhythmia and cardiac remodeling. The present study aimed to evaluate the effects of CRP on NCX1 and intracellular calcium concentration in cardiomyocytes. Primary neonatal mouse ventricular cardiomyocytes were cultured and treated with varying concentrations of CRP (0, 5, 10, 20 and 40 µg/ml). The cardiomyocytes were also treated with NF-κB-specific inhibitor PTDC and a specific inhibitor of the reverse NCX1 KB-R7943 before their intracellular calcium concentrations were measured. mRNA and protein expression levels of NCX1 were detected by reverse transcription-quantitative PCR and western blotting, respectively and intracellular calcium concentration was evaluated by flow cytometry. CRP treatment significantly increased mRNA and protein expression levels of NCX1 in myocytes (P=0.024), as well as intracellular calcium concentration (P=0.01). These results were significantly attenuated by the NF-κB-specific inhibitor PDTC and a specific inhibitor of the reverse NCX1, KB-R7943. CRP significantly upregulated NCX1 expression and increased intracellular calcium concentration in cardiomyocytes via the NF-κB pathway, suggesting that CRP may serve a pro-arrhythmia role via direct influence on the calcium homeostasis of cardiomyocytes.
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Xie et al. (2021) studied Cardiac arrhythmia (in vitro model) (n=200). C-reactive protein (CRP) vs. Control (PBS) was evaluated on mRNA and protein expression levels of NCX1 (p=0.024). CRP treatment significantly increased mRNA and protein expression levels of NCX1 (P=0.024) and intracellular calcium concentration (P=0.01) in cardiomyocytes via the NF-κB pathway.
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