Myocardin-Related Transcription Factor A Is a Common Mediator of Mechanical Stress- and Neurohumoral Stimulation-Induced Cardiac Hypertrophic Signaling Leading to Activation of Brain Natriuretic Peptide Gene Expression

Kuwahara, Koichiro; Kinoshita, Hideyuki; Kuwabara, Yoshihiro; Nakagawa, Yasuaki; Usami, Satoru; Minami, Tetsuto; Yamada, Yuko; Fujiwara, Masataka; Nakao, Kazuwa

doi:10.1128/mcb.00154-10

Cited by 86 publications

(87 citation statements)

References 66 publications

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“…GATA4 is phosphorylated at Ser105 by both ERK and p38,21, 22, 23 regulating its DNA‐binding activity and transcriptional activity 22, 23, 24, 25, 26. In addition to GATA4, a number of other transcriptional regulators, such as nuclear factor of activated T‐cells (NFAT), NKX‐2.5, Elk‐1, activator protein 1, myocardin, serum response factor, and nuclear factor kappa B, have been shown to participate in transcriptional regulation of BNP 20, 27, 28, 29, 30, 31, 32. Several studies have also indicated a central role for M‐CAT element, a thyroid‐responsive element and shear stress‐responsive element on the BNP promoter regulating BNP transcriptional activity 33, 34, 35, 36.…”

Section: Regulation Of Anp and Bnp Gene Expressionmentioning

confidence: 99%

Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

Kerkelä

Ulvila

Magga

2015

JAHA

124

108

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Section: Regulation Of Anp and Bnp Gene Expressionmentioning

confidence: 99%

Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

Kerkelä

Ulvila

Magga

2015

JAHA

124

108

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“…Although the distension of atrial and ventricular cardiomyocytes is generally considered the main mechanical stimulus for the production/secretion of ANP and BNP (57), endothelin-1, ␣-adrenergic agonists, and angiotensin II are also powerful stimulators of production and/or release of CNHs by cardiomyocytes (34,52,67) (Fig. 1 and Table 1).…”

Section: The Regulation Of Gene Expression and Production/secretion Omentioning

confidence: 99%

“…Studies using culture of cardiomyocytes (especially from rodents) have demonstrated that several factors (including calcium, catecholamines, endothelins, angiotensin II, and some cytokines) can regulate the expression of ANP and BNP genes throughout the same transcriptional factors, including p38 mitogen-activated protein kinase (MAPK) (19,34,41,50,52,56,60,91), as indicated in Fig. 1.…”

Section: The Regulation Of Gene Expression and Production/secretion Omentioning

confidence: 99%

Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones

Clerico

Giannoni

Vittorini

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

173

217

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Clerico A, Giannoni A, Vittorini S, Passino C. Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones. Am J Physiol Heart Circ Physiol 301: H12-H20, 2011. First published May 6, 2011; doi:10.1152/ajpheart.00226.2011 reported that atrial extracts contain some biologically active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. It is now clear that the heart also exerts an endocrine function and in this way plays a key role in the regulation of cardiovascular and renal systems. The aim of this review is to discuss some recent insights and still-debated findings regarding the cardiac natriuretic hormones (CNHs) produced and secreted by cardiomyocytes (i.e., atrial natriuretic peptide and B-type natriuretic peptide). The functional status of the CNH system depends not only on the production/secretion of CNHs by cardiomyocytes but also on both the peripheral activation of circulating inactive precursor of natriuretic hormones and the transduction of the hormone signal by specific receptors. In this review, we will discuss the data supporting the hypothesis that the production and secretion of CNHs is the result of a complex integration among mechanical, chemical, hemodynamic, humoral, ischemic, and inflammatory inputs. The cross talk among endocrine function, adipose tissue, and sex steroid hormones will be discussed more in detail, considering the clinically relevant relationships linking together cardiovascular risk, sex, and body fat development and distribution. Finally, we will review the pathophysiological role and the clinical relevance of both peripheral maturation of the precursor of B-type natriuretic peptides and hormone signal transduction.B-type natriuretic peptide; sex steroids; adipokines; heart failure; cardiovascular risk THIRTY YEARS AGO, De Bold et al. (20) reported that atrial extracts contain some biological active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. Several endogenous peptide hormones with natriuretic and vasodilator activity have been identified in the human blood and peripheral tissues (3,30,69,85,86). Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and their related peptides are predominantly produced by atrial and ventricular cardiomyocytes. The term "cardiac natriuretic hormones" (CNHs) will be used in this review to indicate these two families of natriuretic peptides. Another natriuretic peptide, named C-type natriuretic peptide (CNP), is predominantly produced by the endothelial cells, including those of cardiac vessels. Finally, urodilatin is an NH 2 -terminal (NT) 4-amino acid (aa) extented form of ANP, which is produced by the same ANP gene and secreted into the urine by renal tubular cells (16,34,69).From the original observations made 30 years ago, the advances in this particular research field have determined a complete revision about the role of the heart. It is now clear that the heart also exerts a...

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“…All of these elements are known to regulate cardiacspecific gene expression and have been shown to mediate inducible BNP gene expression (13,23). It was also recently shown that a short distance upstream (−193 to −184 in human BNP gene) of this region are CArG-like sequences, which are conserved among different species and mediate hypertrophic stimulus-inducible BNP gene transcription in a SRF-dependent manner (24). Other sites located in more distal regions of the human BNP 5′-FR contain NRSE (−552), shear stress responsive elements (SSREs) (−652, −641, and 161), thyroid hormone responsive element (TRE) (−1000), and nuclear factor of activated T-cells (NF-AT) binding site (−927), which also participate in the inducible activation of the human BNP promoter (Fig.…”

Section: Bnpmentioning

confidence: 99%

“…The 445-bp SM22α promoter, which contains SRF-binding sequences (CArG), a SBE (a Smad-binding site), and a TCE (48,49), is sufficient to direct the expression of a linked reporter gene in cardiac and skeletal muscle during development. In adult hearts, SM22α gene is re-expressed under certain pathological conditions in both mice and humans (24,50). The precise transcriptional mechanisms mediating the re-expression of SM22α in cardiac myocytes in response to pathological stimuli remains unclear, although SRF may be involved, as with cardiac re-expression of SMA.…”

Section: Sm22αmentioning

confidence: 99%

Transcriptional Regulation of the Fetal Cardiac Gene Program

2012

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Abstract. Reactivation of the fetal cardiac gene program in adults is a reliable marker of cardiac hypertrophy and heart failure. Normally, genes within this group are expressed in the fetal ventricles during development, but are silent after birth. However, their expression is re-induced in the ventricular myocardium in response to various cardiovascular diseases, and potentially plays an important role in the pathological process of cardiac remodeling. Thus, analysis of the molecular mechanisms that govern the expression of fetal cardiac genes could lead to the discovery of transcriptional regulators and signaling pathways involved in both cardiac differentiation and cardiac disease. In this review we will summarize what is currently known about the transcriptional regulation of the fetal cardiac gene program.

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Myocardin-Related Transcription Factor A Is a Common Mediator of Mechanical Stress- and Neurohumoral Stimulation-Induced Cardiac Hypertrophic Signaling Leading to Activation of Brain Natriuretic Peptide Gene Expression

Cited by 86 publications

References 66 publications

Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones

Transcriptional Regulation of the Fetal Cardiac Gene Program

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