Cloning and sequence analysis of cDNA encoding a precursor for human brain natriuretic peptide

Sudoh, Tetsuji; Maekawa, Kazuyoshi; Kojima, Masayasu; Minamino, Naoto; Kangawa, Kenji; Matsuo, Hisayuki

doi:10.1016/0006-291x(89)92269-9

Cited by 227 publications

(90 citation statements)

References 14 publications

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“…BNP mRNA is known to harbor a number of putative destabilizing regulatory elements within its 3Ј-untranslated region (40). It has been hypothesized, although not proven, that these elements are responsible for the short half-life (Ͻ1 h) that this transcript exhibits in the intact cardiac myocyte (16).…”

Section: Resultsmentioning

confidence: 99%

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Liang

Garami³

et al. 1997

Journal of Biological Chemistry

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Using a device that applies cyclical strain (1 Hz) to ventricular cardiocytes cultured on collagen-coated silicone elastomer surfaces, we have demonstrated straindependent increases in brain natriuretic peptide (BNP) secretion, BNP mRNA levels, and expression of a transiently transfected ؊1595 human BNP-luciferase reporter. When actinomycin D (10 M) was introduced concomitantly with the strain stimulus, the strain-induced increase in BNP mRNA was eliminated, and the decay of transcripts was identical in the control and strained cells, indicating the lack of independent effects on transcript stability. Strain-dependent ؊1595 human BNPluciferase activity was completely inhibited by chelerythrine, 2-aminopurine, genistein, and W-7 and only partially or not at all by KN-62, wortmannin, and H-89. The effects of these individual agents paralleled their effects on mitogen-activated protein kinase (MAPK) activity, but not c-Jun N-terminal kinase (JNK) activity, in the cells. Overexpression of wild-type MAPK and, to a lesser extent, JNK increased strain-dependent BNP promoter activity, whereas dominant-negative mutants of MAPK kinase, JNK kinase, or Ras completely blocked strain-dependent reporter activity. These findings provide the first demonstration that mechanical strain can increase myocardial gene expression through a transcriptional mechanism and suggest important roles for MAPK and JNK in mediating this effect.The natriuretic peptides comprise a family of vasoactive hormones that play an important role in the regulation of cardiovascular and renal homeostasis (1). Their natriuretic and vasodepressor properties suggest that they represent endogenous antagonists of the various systems (e.g. renin-angiotensin system and sympathetic nervous system) that support arterial blood pressure under basal conditions and, at times, contribute to the pathophysiology of cardiovascular disease.Atrial natriuretic peptide (ANP), 1 the prototype of the group, is produced primarily in the atria of the heart. ANP is expressed in the cardiac ventricle during development and early neonatal life (2, 3). Expression decays as the animal ages and remains quiescent in the adult unless the ventricle is subjected to hemodynamic overload (i.e. mechanical strain that leads to increased wall stress and subsequently to hypertrophy of the myocardium), as occurs with systemic arterial hypertension or congestive heart failure (4 -7).Brain natriuretic peptide (BNP) is also produced in the heart. Despite the nomenclature, relatively little BNP is expressed in the mammalian brain (the exception being the porcine brain, where the peptide was identified originally). Expression of BNP in the heart is lower than that of ANP under basal conditions, and the atrial/ventricular ratio of expression is considerably less than that seen with ANP (8). Ventricular expression of BNP is activated in a fashion similar to ANP in pathophysiological states associated with hemodynamic overload (9, 10). At some stages of advanced congestive heart failure, circulating BNP le...

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Section: Resultsmentioning

confidence: 99%

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Liang

Garami³

et al. 1997

Journal of Biological Chemistry

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“…BNP is synthesized as a 134-amino acid preproBNP precursor, which is cleaved to the 108-amino acid proBNP by removal of a 26-amino acid signal peptide (13 ). A peptide fragment of preproBNP containing amino acid residues 17-26 is present in normal individuals and patients with acute MI.…”

Section: Bnpmentioning

confidence: 99%

“…Of interest, in that study, glycosylation had no impact. In addition, assays specific to the amino terminus (amino acids [11][12][13][14][15][16][17] are less susceptible to BNP cleavage by neprilysin than epitopes specific for amino acids 14 -21. Currently it is not clear how BNP and NT-proBNP concentrations are affected by treatment with LCZ696 in different conditions.…”

Section: Analytics Of Natriuretic Peptide Assaysmentioning

confidence: 99%

Natriuretic Peptides and Analytical Barriers

Vasile

Jaffe

2017

Clinical Chemistry

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BACKGROUND:The natriuretic peptide system is an endocrine, autocrine and paracrine system that plays an important role in the maintenance of cardiovascular homeostasis. Biomarkers based on these peptides are important diagnostic and prognostic tools for myocardial function.CONTENT: Although natriuretic peptides were discovered more than 2 decades ago, their intricate and complex biology is associated with important questions not yet elucidated. The diversity of circulating forms of natriuretic peptides, the distinct expression of these forms in particular patients, and the heterogeneity of heart failure forms, along with specific assay-related and preanalytic issues, cause assays to be poorly harmonized.

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“…Therefore, NT-pro BNP plasma values are approximately six times higher than BNP values. 1,3 The main stimulus responsible for release of BNP is myocardial wall stretch, ventricular dilation, and increased pressures from circulatory volume overload. BNP levels are elevated several-fold in patients with COPD with PH and corpulmonale (COR-P), presumably due to right atrial stretch in response to increased right ventricular afterload.…”

mentioning

confidence: 99%

Plasma Brain Natriuretic Peptide Levels in Chronic Obstructive Pulmonary Disease Patients Without Pulmonary Hypertension

Gupta¹,

Vanane²,

Dubey³

et al. 2018

jebmh

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Cloning and sequence analysis of cDNA encoding a precursor for human brain natriuretic peptide

Cited by 227 publications

References 14 publications

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Natriuretic Peptides and Analytical Barriers

Plasma Brain Natriuretic Peptide Levels in Chronic Obstructive Pulmonary Disease Patients Without Pulmonary Hypertension

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