Transcriptional regulation of the fetal cardiac gene program.

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.

[1]  K. Nakao,et al.  NRSF regulates the fetal cardiac gene program and maintains normal cardiac structure and function , 2003, The EMBO journal.

[2]  Jeffrey Robbins,et al.  A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.

[3]  R. Schwartz,et al.  Sequential activation of alpha-actin genes during avian cardiogenesis: vascular smooth muscle alpha-actin gene transcripts mark the onset of cardiomyocyte differentiation , 1988, The Journal of cell biology.

[4]  Hideki Uosaki,et al.  The cardiac pacemaker-specific channel Hcn4 is a direct transcriptional target of MEF2. , 2009, Cardiovascular research.

[5]  S. Siegelbaum,et al.  Hyperpolarization-activated cation currents: from molecules to physiological function. , 2003, Annual review of physiology.

[6]  K. Nakao,et al.  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 , 2010, Molecular and Cellular Biology.

[7]  J. Seidman,et al.  cis-dominance of rat atrial natriuretic factor gene regulatory sequences in transgenic mice. , 1991, Canadian journal of physiology and pharmacology.

[8]  Christopher P. Regan,et al.  Positive- and Negative-acting Krüppel-like Transcription Factors Bind a Transforming Growth Factor β Control Element Required for Expression of the Smooth Muscle Cell Differentiation Marker SM22α in Vivo * , 2000, The Journal of Biological Chemistry.

[9]  Kazuwa Nakao,et al.  Regulation and significance of atrial and brain natriuretic peptides as cardiac hormones. , 2010, Endocrine journal.

[10]  J. Vandekerckhove,et al.  Actin isoform expression patterns during mammalian development and in pathology: insights from mouse models. , 2009, Cell motility and the cytoskeleton.

[11]  L. Karns,et al.  M-CAT, CArG, and Sp1 elements are required for alpha 1-adrenergic induction of the skeletal alpha-actin promoter during cardiac myocyte hypertrophy. Transcriptional enhancer factor-1 and protein kinase C as conserved transducers of the fetal program in cardiac growth. , 1995, The Journal of biological chemistry.

[12]  Raquel P. Ritchie,et al.  Myocardin Enhances Smad3-Mediated Transforming Growth Factor-β1 Signaling in a CArG Box-Independent Manner: Smad-Binding Element Is an Important cis Element for SM22α Transcription In Vivo , 2005, Circulation research.

[13]  Thomas Thum,et al.  MicroRNAs in the Human Heart: A Clue to Fetal Gene Reprogramming in Heart Failure , 2007 .

[14]  G. Owens,et al.  Positive- and negative-acting Kruppel-like transcription factors bind a transforming growth factor beta control element required for expression of the smooth muscle cell differentiation marker SM22alpha in vivo. , 2000, The Journal of biological chemistry.

[15]  Inducible regulation of human brain natriuretic peptide promoter in transgenic mice. , 2001 .

[16]  倉富 忍,et al.  NRSF regulates the developmental and hypertrophic changes of HCN4 transcription in rat cardiac myocytes , 2008 .

[17]  M. Garami,et al.  Tissue-specific expression of the human brain natriuretic peptide gene in cardiac myocytes. , 1996, Hypertension.

[18]  S. Ertel,et al.  Voltage-gated T-type Ca2+ channels and heart failure. , 1999, Proceedings of the Association of American Physicians.

[19]  N. Tamura,et al.  Two cardiac natriuretic peptide genes (atrial natriuretic peptide and brain natriuretic peptide) are organized in tandem in the mouse and human genomes. , 1996, Journal of molecular and cellular cardiology.

[20]  E. Olson,et al.  A family of microRNAs encoded by myosin genes governs myosin expression and muscle performance. , 2009, Developmental cell.

[21]  T. Lee,et al.  Transforming growth factor-beta response elements of the skeletal alpha-actin gene. Combinatorial action of serum response factor, YY1, and the SV40 enhancer-binding protein, TEF-1. , 1994, The Journal of biological chemistry.

[22]  A. J. Bold,et al.  Determinants of inducible brain natriuretic peptide promoter activity , 2005, Regulatory Peptides.

[23]  K. Nakao,et al.  The Neuron-Restrictive Silencer Element–Neuron-Restrictive Silencer Factor System Regulates Basal and Endothelin 1-Inducible Atrial Natriuretic Peptide Gene Expression in Ventricular Myocytes , 2001, Molecular and Cellular Biology.

[24]  B. Greenberg,et al.  Upstream sequences confer atrial-specific expression on the human atrial natriuretic factor gene. , 1988, The Journal of biological chemistry.

[25]  R. Schwartz,et al.  The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load. , 1991, The Journal of clinical investigation.

[26]  L. Field,et al.  Atrial natriuretic factor-SV40 T antigen transgenes produce tumors and cardiac arrhythmias in mice. , 1988, Science.

[27]  M. Nemer,et al.  The Zinc Finger-Only Protein Zfp260 Is a Novel Cardiac Regulator and a Nuclear Effector of α1-Adrenergic Signaling , 2005, Molecular and Cellular Biology.

[28]  T. Opthof,et al.  Cav3.2 subunit underlies the functional T-type Ca2+ channel in murine hearts during the embryonic period. , 2004, American journal of physiology. Heart and circulatory physiology.

[29]  P. Townsend,et al.  Molecular regulation of cardiac hypertrophy. , 2008, The international journal of biochemistry & cell biology.

[30]  C. Glembotski,et al.  Stabilization of the B-type natriuretic peptide mRNA in cardiac myocytes by alpha-adrenergic receptor activation: potential roles for protein kinase C and mitogen-activated protein kinase. , 1996, Molecular endocrinology.

[31]  T. Opthof,et al.  Pathophysiological significance of T-type Ca2+ channels: expression of T-type Ca2+ channels in fetal and diseased heart. , 2005, Journal of pharmacological sciences.

[32]  C. Wahl-Schott,et al.  HCN channels: Structure, cellular regulation and physiological function , 2009, Cellular and Molecular Life Sciences.

[33]  Xiaoxia Qi,et al.  Gene Expression by a MicroRNA Control of Stress-Dependent Cardiac Growth , 2008 .

[34]  K. Nakao,et al.  Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload. , 1995, The Journal of clinical investigation.

[35]  G. Owens,et al.  Molecular regulation of vascular smooth muscle cell differentiation in development and disease. , 2004, Physiological reviews.

[36]  Kyoichi Ono,et al.  Cardiac T-type Ca(2+) channels in the heart. , 2010, Journal of molecular and cellular cardiology.

[37]  R. Schwartz,et al.  Differential regulation of skeletal alpha-actin transcription in cardiac muscle by two fibroblast growth factors. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[38]  S. Nattel,et al.  Molecular basis of funny current (If) in normal and failing human heart. , 2008, Journal of molecular and cellular cardiology.

[39]  E. Olson,et al.  SM22 alpha, a marker of adult smooth muscle, is expressed in multiple myogenic lineages during embryogenesis. , 1996, Circulation research.

[40]  J. Drouin,et al.  Developmental stage-specific regulation of atrial natriuretic factor gene transcription in cardiac cells , 1994, Molecular and cellular biology.

[41]  N. Tamura,et al.  Characterization of the 5′-flanking region and chromosomal assignment of the human brain natriuretic peptide gene , 1995, Journal of Molecular Medicine.

[42]  C. Seidman,et al.  Divergent pathways mediate the induction of ANF transgenes in neonatal and hypertrophic ventricular myocardium. , 1995, The Journal of clinical investigation.

[43]  G. Owens,et al.  Regulation of smooth muscle alpha-actin expression in vivo is dependent on CArG elements within the 5' and first intron promoter regions. , 1999, Circulation research.

[44]  A. Mugelli,et al.  I(f) in non-pacemaker cells: role and pharmacological implications. , 2006, Pharmacological research.

[45]  M. Lapointe Molecular regulation of the brain natriuretic peptide gene , 2005, Peptides.

[46]  T. Parker,et al.  Peptide growth factors can provoke "fetal" contractile protein gene expression in rat cardiac myocytes. , 1990, The Journal of clinical investigation.

[47]  A. Moorman,et al.  Expression and regulation of the atrial natriuretic factor encoding gene Nppa during development and disease. , 2005, Cardiovascular research.

[48]  John McAnally,et al.  TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling. , 2006, The Journal of clinical investigation.

[49]  E. Olson A decade of discoveries in cardiac biology , 2004, Nature Medicine.

[50]  D. Gardner,et al.  Molecular biology of the natriuretic peptide system: implications for physiology and hypertension. , 2007, Hypertension.

[51]  C. Orosz,et al.  Serum response factor neutralizes Pur-and Pur -mediated repression of the fetal vascular smooth muscle -actin gene in stressed adult cardiomyocytes , 2008 .