Expression of C-type natriuretic peptide and its receptor NPR-B in cardiomyocytes

Ry, Silvia Del; Cabiati, Manuela; Vozzi, Federico; Battolla, Barbara; Caselli, Chiara; Forini, Francesca; Segnani, Cristina; Prescimone, Tommaso; Giannessi, Daniela; Mattii, Letizia

doi:10.1016/j.peptides.2011.06.014

Cited by 69 publications

(34 citation statements)

References 36 publications

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“…Immunohistochemistry, used to evaluate CNP expression, was carried out as previously described [42]. Briefly, after antigen retrieval and endogenous peroxidases/non specific binding blocking, the samples were incubated with a rabbit anti-CNP antibody (CNP-53, Phoenix Pharmaceuticals, Inc., CA, USA) diluted 1∶800 in 1% bovine serum albumin/phosphate buffered saline (BSA/PBS).…”

Section: Methodsmentioning

confidence: 99%

Impact of Obesity on the Expression Profile of Natriuretic Peptide System in a Rat Experimental Model

et al. 2013

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Natriuretic peptides (NPs) play an important role in obesity and aim of this study was to evaluate, in cardiac tissue of obese Zucker rats (O, n = 29) their transcriptomic profile compared to controls (CO, n = 24) by Real-Time PCR study; CNP protein expression was evaluated by immunostaining and immunometric tests. Myocardial histology was performed, confirming no alteration of organ structure. While ANP and BNP are cardiac peptides, CNP is mainly an endothelial hormone; thus its expression, as well as that of NPR-B and NPR-C, was also evaluated in kidney and lung of an animal subgroup (n = 20). In heart, lower BNP mRNA levels in O vs CO (p = 0.02) as well as ANP and CNP (p = ns), were detected. NPR-B/NPR-A mRNA was similar in O and CO, while NPR-C was numerically lower (p = ns) in O than in CO. In kidney, CNP/NPR-B/NPR-C mRNA was similar in O and CO, while in lung CNP/NPR-C expression decreased and NPR-B increased (p = ns) in O vs CO. Subdividing into fasting and hyperglycemic rats, the pattern of mRNA expression for each gene analyzed remained unchanged. The trend observed in heart, kidney and lung for CNP protein concentrations and immunohistochemistry reflected the mRNA expression. TNF-α and IL-6 mRNA were measured in each tissue and no significant genotype effect was detected in any tissue. The main NP variations were observed at the cardiac level, suggesting a reduced release by cardiac cells. The understanding of mechanisms involved in the modulation of the NP system in obesity could be a useful starting point for future clinical study devoted to identifying new obesity treatment strategies.

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Section: Methodsmentioning

confidence: 99%

Impact of Obesity on the Expression Profile of Natriuretic Peptide System in a Rat Experimental Model

et al. 2013

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“…Myocardial tissue samples were paraffin-embedded, cut into 5-µm-thick sections, mounted serially on glass slides and treated for immunohistochemistry as previously described [18].…”

Section: Methodsmentioning

confidence: 99%

Pacing-Induced Regional Differences in Adenosine Receptors mRNA Expression in a Swine Model of Dilated Cardiomyopathy

Cabiati

Lionetti

et al. 2012

PLoS ONE

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The adenosinergic system is essential in the mediation of intrinsic protection and myocardial resistance to insult; it may be considered a cardioprotective molecule and adenosine receptors (ARs) represent potential therapeutic targets in the setting of heart failure (HF). The aim of the study was to test whether differences exist between mRNA expression of ARs in the anterior left ventricle (LV) wall (pacing site: PS) compared to the infero septal wall (opposite region: OS) in an experimental model of dilated cardiomyopathy. Cardiac tissue was collected from LV PS and OS of adult male minipigs with pacing-induced HF (n = 10) and from a control group (C, n = 4). ARs and TNF–α mRNA expression was measured by Real Time-PCR and the results were normalized with the three most stably expressed genes (GAPDH, HPRT1, TBP). Immunohistochemistry analysis was also performed. After 3 weeks of pacing higher levels of expression for each analyzed AR were observed in PS except for A1R (A1R: C = 0.6±0.2, PS = 0.1±0.04, OS = 0.04±0.01, p<0.0001 C vs. PS and OS respectively; A2AR: C = 1.04±0.59, PS = 2.62±0.79, OS = 2.99±0.79; A2BR: C = 1.2±0.1, PS = 5.59±2.3, OS = 1.59±0.46; A3R: C = 0.76±0.18, PS = 8.40±3.38, OS = 4.40±0.83). Significant contractile impairment and myocardial hypoperfusion were observed at PS after three weeks of pacing as compared to OS. TNF-α mRNA expression resulted similar in PS (6.3±2.4) and in OS (5.9±2.7) although higher than in control group (3.4±1.5). ARs expression was mainly detected in cardiomyocytes. This study provided new information on ARs local changes in the setting of LV dysfunction and on the role of these receptors in relation to pacing-induced abnormalities of myocardial perfusion and contraction. These results suggest a possible therapeutic role of adenosine in patients with HF and dyssynchronous LV contraction.

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“…CNP expression has also been detected in cardiomyocytes [19], vascular endothelium [20], and bone [21]. Among the family of natriuretic peptides, CNP is the most highly conserved between species and may in fact represent the ancestral precursor from which atrial (ANP) and B-type (BNP) natriuretic peptides evolved [22, 23].…”

Section: C-type Natriuretic Peptide Biologymentioning

confidence: 99%

Urinary C-type natriuretic peptide: An emerging biomarker for heart failure and renal remodeling

Zakeri

Burnett

Sangaralingham

2015

Clinica Chimica Acta

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The public health and economic burden of heart failure (HF) is staggering and the need for relevant pathophysiologic and clinical biomarkers to advance the field and improve HF therapy remains high. Renal dysfunction is common among HF patients and is associated with increased HF hospitalization and mortality. It is widely recognized that mechanisms contributing to HF pathogenesis include a complex bidirectional interaction between the kidney and heart, encompassed by the term cardiorenal syndrome (CRS). Among a new wave of urinary biomarkers germane to CRS, C-type natriuretic peptide (CNP) has emerged as an innovative biomarker of renal structural and functional impairment in HF and chronic renal disease states. CNP is a hormone, synthesized in the kidney, and is an important regulator of cell proliferation and organ fibrosis. Hypoxia, cytokines and fibrotic growth factors, which are inherent to both cardiac and renal remodeling processes, are among the recognized stimuli for CNP production and release. In this review we aim to highlight current knowledge regarding the biology and pathophysiologic correlates of urinary CNP, and its potential clinical utility as a diagnostic and prognostic biomarker in HF and renal disease states.

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Expression of C-type natriuretic peptide and its receptor NPR-B in cardiomyocytes

Cited by 69 publications

References 36 publications

Impact of Obesity on the Expression Profile of Natriuretic Peptide System in a Rat Experimental Model

Impact of Obesity on the Expression Profile of Natriuretic Peptide System in a Rat Experimental Model

Pacing-Induced Regional Differences in Adenosine Receptors mRNA Expression in a Swine Model of Dilated Cardiomyopathy

Urinary C-type natriuretic peptide: An emerging biomarker for heart failure and renal remodeling

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