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Article

Opposing Roles of FoxP1 and Nfat3 in Transcriptional Control of Cardiomyocyte Hypertrophy

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Pages 3068-3080 | Received 10 Aug 2010, Accepted 09 May 2011, Published online: 20 Mar 2023

REFERENCES

  • Abraham, W. T., et al. 2002. Coordinate changes in myosin heavy chain isoform gene expression are selectively associated with alterations in dilated cardiomyopathy phenotype. Mol. Med. 8:750–760.
  • Barry, S. P., S. M. Davidson, and P. A. Townsend. 2008. Molecular regulation of cardiac hypertrophy. Int. J. Biochem. Cell Biol. 40:2023–2039.
  • Bettelli, E., M. Dastrange, and M. Oukka. 2005. Foxp3 interacts with nuclear factor of activated T cells and NF-kappa B to repress cytokine gene expression and effector functions of T helper cells. Proc. Natl. Acad. Sci. U. S. A. 102:5138–5143.
  • Bushdid, P. B., H. Osinska, R. R. Waclaw, J. D. Molkentin, and K. E. Yutzey. 2003. NFATc3 and NFATc4 are required for cardiac development and mitochondrial function. Circ. Res. 92:1305–1313.
  • Chen, L., J. N. Glover, P. G. Hogan, A. Rao, and S. C. Harrison. 1998. Structure of the DNA-binding domains from NFAT, Fos and Jun bound specifically to DNA. Nature 392:42–48.
  • de la Pompa, J. L., et al. 1998. Role of the NF-ATc transcription factor in morphogenesis of cardiac valves and septum. Nature 392:182–186.
  • Diebold, R. J., N. Rajaram, D. A. Leonard, and T. K. Kerppola. 1998. Molecular basis of cooperative DNA bending and oriented heterodimer binding in the NFAT1-Fos-Jun-ARRE2 complex. Proc. Natl. Acad. Sci. U. S. A. 95:7915–7920.
  • Dodge, S. M., et al. 1998. Effects of angiotensin II on expression of the gap junction channel protein connexin43 in neonatal rat ventricular myocytes. J. Am. Coll. Cardiol. 32:800–807.
  • Dorn, G. W.II, J. Robbins, N. Ball, and R. A. Walsh. 1994. Myosin heavy chain regulation and myocyte contractile depression after LV hypertrophy in aortic-banded mice. Am. J. Physiol. 267:H400–H405.
  • Dostal, D. E., and K. M. Baker. 1992. Angiotensin II stimulation of left ventricular hypertrophy in adult rat heart. Mediation by the AT1 receptor. Am. J. Hypertens. 5:276–280.
  • Evans-Anderson, H. J., C. M. Alfieri, and K. E. Yutzey. 2008. Regulation of cardiomyocyte proliferation and myocardial growth during development by FOXO transcription factors. Circ. Res. 102:686–694.
  • Giffin, M. J., et al. 2003. Structure of NFAT1 bound as a dimer to the HIV-1 LTR kappa B element. Nat. Struct. Biol. 10:800–806.
  • Graef, I. A., F. Chen, L. Chen, A. Kuo, and G. R. Crabtree. 2001. Signals transduced by Ca(2+)/calcineurin and NFATc3/c4 pattern the developing vasculature. Cell 105:863–875.
  • Gwathmey, J. K., et al. 1987. Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. Circ. Res. 61:70–76.
  • Haley, S. A., et al. 2008. Forced expression of the cell cycle inhibitor p57Kip2 in cardiomyocytes attenuates ischemia-reperfusion injury in the mouse heart. BMC Physiol. 8:4.
  • Hannenhalli, S., et al. 2006. Transcriptional genomics associates FOX transcription factors with human heart failure. Circulation 114:1269–1276.
  • Heineke, J., and J. D. Molkentin. 2006. Regulation of cardiac hypertrophy by intracellular signalling pathways. Nat. Rev. Mol. Cell Biol. 7:589–600.
  • Hu, C. D., Y. Chinenov, and T. K. Kerppola. 2002. Visualization of interactions among bZIP and Rel family proteins in living cells using bimolecular fluorescence complementation. Mol. Cell 9:789–798.
  • Hu, H., et al. 2006. Foxp1 is an essential transcriptional regulator of B cell development. Nat. Immunol. 7:819–826.
  • Huang, Y., H. Liu, and Y. Li. 2001. Alterations in myosin heavy chain isoform gene expression during the transition from compensatory hypertrophy to congestive heart failure in rats. Chin. Med. J. (Engl.) 114:183–185.
  • James, J., et al. 2005. Forced expression of alpha-myosin heavy chain in the rabbit ventricle results in cardioprotection under cardiomyopathic conditions. Circulation 111:2339–2346.
  • Jepsen, K., A. S. Gleiberman, C. Shi, D. I. Simon, and M. G. Rosenfeld. 2008. Cooperative regulation in development by SMRT and FOXP1. Genes Dev. 22:740–745.
  • Krenz, M., and J. Robbins. 2004. Impact of beta-myosin heavy chain expression on cardiac function during stress. J. Am. Coll. Cardiol. 44:2390–2397.
  • Li, S., D. Zhou, M. M. Lu, and E. E. Morrisey. 2004. Advanced cardiac morphogenesis does not require heart tube fusion. Science 305:1619–1622.
  • Lim, H. W., et al. 2000. Reversal of cardiac hypertrophy in transgenic disease models by calcineurin inhibition. J. Mol. Cell. Cardiol. 32:697–709.
  • McCaffrey, P. G., et al. 1993. Isolation of the cyclosporin-sensitive T cell transcription factor NFATp. Science 262:750–754.
  • Miyata, S., W. Minobe, M. R. Bristow, and L. A. Leinwand. 2000. Myosin heavy chain isoform expression in the failing and nonfailing human heart. Circ. Res. 86:386–390.
  • Molkentin, J. D., et al. 1998. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 93:215–228.
  • Müller, O. J., et al. 2003. Transgenic rat hearts overexpressing SERCA2a show improved contractility under baseline conditions and pressure overload. Cardiovasc. Res. 59:380–389.
  • Ni, Y. G., et al. 2006. Foxo transcription factors blunt cardiac hypertrophy by inhibiting calcineurin signaling. Circulation 114:1159–1168.
  • Papanicolaou, K. N., Y. Izumiya, and K. Walsh. 2008. Forkhead transcription factors and cardiovascular biology. Circ. Res. 102:16–31.
  • Ramirez-Carrozzi, V., and T. Kerppola. 2003. Asymmetric recognition of nonconsensus AP-1 sites by Fos-Jun and Jun-Jun influences transcriptional cooperativity with NFAT1. Mol. Cell. Biol. 23:1737–1749.
  • Ranger, A. M., et al. 1998. The transcription factor NF-ATc is essential for cardiac valve formation. Nature 392:186–190.
  • Roos, K. P., et al. 2007. Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger. J. Card. Fail. 13:318–329.
  • Rössler, O. G., I. Henss, and G. Thiel. 2008. Transcriptional response to muscarinic acetylcholine receptor stimulation: regulation of Egr-1 biosynthesis by ERK, Elk-1, MKP-1, and calcineurin in carbachol-stimulated human neuroblastoma cells. Arch. Biochem. Biophys. 470:93–102.
  • Rothermel, B. A., et al. 2001. Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo. Proc. Natl. Acad. Sci. U. S. A. 98:3328–3333.
  • Sakai, S., et al. 1998. Altered expression of isoforms of myosin heavy chain mRNA in the failing rat heart is ameliorated by chronic treatment with an endothelin receptor antagonist. J. Cardiovasc. Pharmacol. 31(Suppl. 1):S302–S305.
  • Schunkert, H., et al. 1990. Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation. J. Clin. Invest. 86:1913–1920.
  • Sengupta, A., J. D. Molkentin, and K. E. Yutzey. 2009. FoxO transcription factors promote autophagy in cardiomyocytes. J. Biol. Chem. 284:28319–28331.
  • Severs, N. J., A. F. Bruce, E. Dupont, and S. Rothery. 2008. Remodelling of gap junctions and connexin expression in diseased myocardium. Cardiovasc. Res. 80:9–19.
  • Skurk, C., et al. 2005. The FOXO3a transcription factor regulates cardiac myocyte size downstream of AKT signaling. J. Biol. Chem. 280:20814–20823.
  • Smyth, J. W., et al. 2010. Limited forward trafficking of connexin 43 reduces cell-cell coupling in stressed human and mouse myocardium. J. Clin. Invest. 120:266–279.
  • Stroud, J. C., et al. 2006. Structure of the forkhead domain of FOXP2 bound to DNA. Structure 14:159–166.
  • Sundrud, M. S., and A. Rao. 2007. New twists of T cell fate: control of T cell activation and tolerance by TGF-beta and NFAT. Curr. Opin. Immunol. 19:287–293.
  • van Rooij, E., et al. 2004. MCIP1 overexpression suppresses left ventricular remodeling and sustains cardiac function after myocardial infarction. Circ. Res. 94:e18–e26.
  • Vega, R. B., et al. 2003. Dual roles of modulatory calcineurin-interacting protein 1 in cardiac hypertrophy. Proc. Natl. Acad. Sci. U. S. A. 100:669–674.
  • Wang, B., D. Lin, C. Li, and P. Tucker. 2003. Multiple domains define the expression and regulatory properties of Foxp1 forkhead transcriptional repressors. J. Biol. Chem. 278:24259–24268.
  • Wang, B., et al. 2004. Foxp1 regulates cardiac outflow tract, endocardial cushion morphogenesis and myocyte proliferation and maturation. Development 131:4477–4487.
  • Wang, Y., et al. 2002. Direct biomechanical induction of endogenous calcineurin inhibitor Down Syndrome Critical Region-1 in cardiac myocytes. Am. J. Physiol. Heart Circ. Physiol. 283:H533–H539.
  • Wildin, R. S., et al. 2001. X-linked neonatal diabetes mellitus, enteropathy and endocrinopathy syndrome is the human equivalent of mouse scurfy. Nat. Genet. 27:18–20.
  • Wright, C. E., P. W. Bodell, F. Haddad, A. X. Qin, and K. M. Baldwin. 2001. In vivo regulation of the beta-myosin heavy chain gene in hypertensive rodent heart. Am. J. Physiol. Cell Physiol. 280:C1262–C1276.
  • Wu, X., P. Eder, B. Chang, and J. D. Molkentin. 2010. TRPC channels are necessary mediators of pathologic cardiac hypertrophy. Proc. Natl. Acad. Sci. U. S. A. 107:7000–7005.
  • Wu, Y., et al. 2006. FOXP3 controls regulatory T cell function through cooperation with NFAT. Cell 126:375–387.
  • Yang, J., et al. 2000. Independent signals control expression of the calcineurin inhibitory proteins MCIP1 and MCIP2 in striated muscles. Circ. Res. 87:E61–E68.
  • Zhang, Y., et al. 2010. Foxp1 coordinates cardiomyocyte proliferation through both cell-autonomous and nonautonomous mechanisms. Genes Dev. 24:1746–1757.

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