C-Reactive Protein Causes Blood Pressure Drop in Rabbits and Induces Intracellular Calcium Signaling

Bock, C.; Vogt, Birgit; Mattecka, Stephan; Yapici, Gülcan; Brunner, Patrizia; Fimpel, Sandra; Unger, Juliane K.; Sheriff, Ahmed

doi:10.3389/fimmu.2020.01978

Cited by 7 publications

(11 citation statements)

References 44 publications

(35 reference statements)

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“…One of these recent studies showed a direct, quick and extreme effect of CRP on blood pressure in rabbits (61). Human CRP was intravenously injected in vivo to reach a level of 50 mg/L.…”

Section: Crp Has An Effect On Blood Pressurementioning

confidence: 99%

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C-Reactive Protein Triggers Cell Death in Ischemic Cells

Sheriff

Kayser

Brunner³

et al. 2021

Front. Immunol.

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C-reactive protein (CRP) is the best-known acute phase protein. In humans, almost every type of inflammation is accompanied by an increase of CRP concentration. Until recently, the only known physiological function of CRP was the marking of cells to initiate their phagocytosis. This triggers the classical complement pathway up to C4, which helps to eliminate pathogens and dead cells. However, vital cells with reduced energy supply are also marked, which is useful in the case of a classical external wound because an important substrate for pathogens is disposed of, but is counterproductive at internal wounds (e.g., heart attack or stroke). This mechanism negatively affects clinical outcomes since it is established that CRP levels correlate with the prognosis of these indications. Here, we summarize what we can learn from a clinical study in which CRP was adsorbed from the bloodstream by CRP-apheresis. Recently, it was shown that CRP can have a direct effect on blood pressure in rabbits. This is interesting in regard to patients with high inflammation, as they often become tachycardic and need catecholamines. These two physiological effects of CRP apparently also occur in COVID-19. Parts of the lung become ischemic due to intra-alveolar edema and hemorrhage and in parallel CRP increases dramatically, hence it is assumed that CRP is also involved in this ischemic condition. It is meanwhile considered that most of the damage in COVID-19 is caused by the immune system. The high amounts of CRP could have an additional influence on blood pressure in severe COVID-19.

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“…One of these recent studies showed a direct, quick and extreme effect of CRP on blood pressure in rabbits (61). Human CRP was intravenously injected in vivo to reach a level of 50 mg/L.…”

Section: Crp Has An Effect On Blood Pressurementioning

confidence: 99%

“…After seeing such a dramatic drop in blood pressure the influence of CRP on AR signal transduction was investigated in vitro (61). ARs signal via calcium (Ca 2+ ) as second messenger was measured in real-time.…”

Section: Crp Has An Effect On Blood Pressurementioning

confidence: 99%

C-Reactive Protein Triggers Cell Death in Ischemic Cells

Sheriff

Kayser

Brunner³

et al. 2021

Front. Immunol.

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“…Publications in recent years showed that CRP is more than a biomarker and affects both physiological and pathological processes [5,[7][8][9]. The direct influence of CRP on the cardiovascular system of rabbits has been reported recently [10]. Here, the infusion of human CRP led to a sharp drop in blood pressure within seconds, while the heart rate was not affected.…”

Section: Introductionmentioning

confidence: 79%

“…Human CRP (Pentracor, Hennigsdorf, Germany) was purified from human pooled plasma with a selective CRP-binding matrix as described elsewhere in detail [10]. Endotoxin contamination was avoided, and CRP was stored in its native, pentameric form.…”

Section: Pharmacological Agonists and Crpmentioning

confidence: 99%

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C-Reactive Protein (CRP) Blocks the Desensitization of Agonistic Stimulated G Protein Coupled Receptors (GPCRs) in Neonatal Rat Cardiomyocytes

Wallukat¹,

Mattecka

Wenzel³

et al. 2022

JCM

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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.

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