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Abstract
Recently, C-reactive protein (CRP) was shown to affect intracellular calcium signaling and blood pressure in vitro and in vivo, respectively. The aim of the present study was to further investigate if a direct effect on G-protein coupled receptor (GPCR) signaling by CRP can be observed by using CRP in combination with different GPCR agonists on spontaneously beating cultured neonatal rat cardiomyocytes. All used agonists (isoprenaline, clenbuterol, phenylephrine, angiotensin II and endothelin 1) affected the beat rate of cardiomyocytes significantly and after washing them out and re-stimulation the cells developed a pronounced desensitization of the corresponding receptors. CRP did not affect the basal beating-rate nor the initial increase/decrease in beat-rate triggered by different agonists. However, CRP co-incubated cells did not exhibit desensitization of the respective GPCRs after the stimulation with the different agonists. This lack of desensitization was independent of the GPCR type, but it was dependent on the CRP concentration. Therefore, CRP interferes with the desensitization of GPCRs and has to be considered as a novel regulator of adrenergic, angiotensin-1 and endothelin receptors.
Highlights
The homopentameric C-reactive protein (CRP) is a classic acute phase protein that has been known in human medicine for decades
With additional CRP incubation, the cardiomyocyte beating rate increased to a similar level compared to the initial stimulation and was significantly higher compared to the control experiment
Cells that were treated with CRP preincubated with a monoclonal antibody to inhibit the CRP action showed normal desensitization and a beating rate comparable to that in ISO stimulated cells alone after 130 min (Figure 1A)
Summary
The homopentameric C-reactive protein (CRP) is a classic acute phase protein that has been known in human medicine for decades. It has been established primarily as a biomarker for active and chronic inflammation of bacterial origin [1] This picture has changed fundamentally. Low blood levels at >2 mg/L CRP are associated with an increased risk of heart attack, stroke, diabetes and mortality depending on the concentration that was observed [2,3,4]. Acute inflammation caused by vessel occlusions can be observed in acute myocardial infarction, with rapidly increasing CRP levels up to >100 mg/L over 2–4 days. Restrictions of organic functions may be the consequences of CRP mediated ischemic processes [5,6]
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