Skip to main content
SpringerLink
Log in

Mechanisms for the Regulation of Phospholipase C Gene Expression in Cardiac Hypertrophy

  • Chapter
  • First Online:
Molecular Defects in Cardiovascular Disease

  • 607 Accesses

Abstract

Phospholipase C (PLC) is considered to mediate the cardiomyocyte hypertrophic response to norepinephrine. However, a paucity of information exists regarding the regulation of specific PLC isozyme gene and ­protein expression as well as activities in normal and hypertrophied myocardium. In this chapter, the role of PLC isozymes in cardiac hypertrophy as well as some of the mechanisms that are involved in the regulation of PLC isozyme gene expression, protein abundance and activities are discussed. On the basis of the available literature, it is suggested that specific PLC isozymes could be involved in the cardiomyocyte response to different hypertrophic stimuli and that modification of the transcriptional regulation of PLC isozymes could also prevent the progression of cardiac hypertrophy and its transition to heart failure.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 89.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 119.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Opie LH. The heart: physiology, from cell to circulation. 3rd ed. New York: Lippincott-Raven; 1998.

    Google Scholar 

  2. Lamers JM, De Jonge HW, Panagia V, et al. Receptor-mediated signalling pathways acting through hydrolysis of membrane phospholipids in cardiomyocytes. Cardioscience. 1993;4:121–31.

    PubMed  CAS  Google Scholar 

  3. Izumo S, Aoki H. Calcineurin – the missing link in cardiac hypertrophy. Nat Med. 1998;4:661–2.

    Article  PubMed  CAS  Google Scholar 

  4. Tappia PS, Singal T, Dent MR, et al. Phospholipid-mediated signaling in diseased myocardium. Future Lipidol. 2006;1:701–17.

    Article  CAS  Google Scholar 

  5. Tappia PS, Dent MR, Dhalla NS. Oxidative stress and redox regulation of phospholipase D in myocardial disease. Free Radic Biol Med. 2006;41:349–61.

    Article  PubMed  CAS  Google Scholar 

  6. Tappia PS. Phospholipid-mediated signaling systems as novel targets for treatment of heart disease. Can J Physiol Pharmacol. 2007;85:25–41.

    Article  PubMed  CAS  Google Scholar 

  7. Rhee SG. Regulation of phosphoinositide-specific phospholipase C. Annu Rev Biochem. 2001;70:281–312.

    Article  PubMed  CAS  Google Scholar 

  8. Singal T, Dhalla NS, Tappia PS. Phospholipase C may be involved in norepinephrine-induced cardiac hypertrophy. Biochem Biophys Res Commun. 2004;320:1015–9.

    Article  PubMed  CAS  Google Scholar 

  9. Singal T, Dhalla NS, Tappia PS. Norepinephrine-induced changes in gene expression of phospholipase C in cardiomyocytes. J Mol Cell Cardiol. 2006;41:126–37.

    Article  PubMed  CAS  Google Scholar 

  10. Tappia PS, Padua RR, Panagia V, et al. Fibroblast growth factor-2 stimulates phospholipase C β in adult cardiomyocytes. Biochem Cell Biol. 1999;77:569–75.

    Article  PubMed  CAS  Google Scholar 

  11. Guo Y, Rebecchi M, Scariata S. Phospholipase C β2 binds to and inhibits phospholipase C δ1. J Biol Chem. 2005;280:1438–47.

    Article  PubMed  CAS  Google Scholar 

  12. Fukami K. Structure, regulation, and function of phospholipase C isozymes. J Biochem. 2002;131:293–9.

    PubMed  CAS  Google Scholar 

  13. James SR, Downes CP. Structural and mechanistic features of phospholipases C: effectors of inositol phospholipid-mediated signal transduction. Cell Signal. 1997;9:329–36.

    Article  PubMed  CAS  Google Scholar 

  14. Lopez I, Mak EC, Ding J, et al. A novel bifunctional phospholipase C that is regulated by Gα12 and stimulates the Ras/mitogen-activated protein kinase pathway. J Biol Chem. 2001;276:2758–65.

    Article  PubMed  CAS  Google Scholar 

  15. Heredia Mdel P, Delgado C, Pereira L, et al. Neuropeptide Y rapidly enhances [Ca2+]i transients and Ca2+ sparks in adult rat ventricular myocytes through Y1 receptor and PLC activation. J Mol Cell Cardiol. 2005;38:205–12.

    Article  PubMed  CAS  Google Scholar 

  16. Balogh J, Wihlborg AK, Isackson H, et al. Phospholipase C and cAMP-dependent positive inotropic effects of ATP in mouse cardiomyocytes via P2Y11-like ­receptors. J Mol Cell Cardiol. 2005;39:223–30.

    Article  PubMed  CAS  Google Scholar 

  17. Yin G, Yan C, Berk BC. Angiotensin II signaling pathways mediated by tyrosine kinases. Int J Biochem Cell Biol. 2003;35:780–3.

    Article  PubMed  CAS  Google Scholar 

  18. Kockskämper J, Zima AV, Roderick HL, et al. Emerging roles of inositiol 1,4,5-trisphosphate signaling in cardiac myocytes. J Mol Cell Cardiol. 2008;45:128–47.

    Article  PubMed  CAS  Google Scholar 

  19. Vasilevski O, Grubb DR, Filtz TM, et al. Ins(1,4,5)P3 regulates phospholipase C β1 expression in cardiomyocytes. J Mol Cell Cardiol. 2008;45:679–84.

    Article  PubMed  CAS  Google Scholar 

  20. Wu X, Zhang T, Bossuyt J, et al. Local InsP3-dependent perinuclear Ca2+ signaling in cardiac myocyte excitation-transcription coupling. J Clin Invest. 2006;116:675–82.

    Article  PubMed  CAS  Google Scholar 

  21. Bers DM. Cardiac excitation-contraction coupling. Nature. 2002;415:198–205.

    Article  PubMed  CAS  Google Scholar 

  22. Mackenzie L, Bootman MD, Laine M, et al. The role of inositol 1,4,5-trisphosphate receptors in Ca2+ signaling and the generation of arrhythmias in rat atrial myocytes. J Physiol. 2004;555:395–409.

    Google Scholar 

  23. Zima AV, Blatter LA. Inositol 1,4,5-trisphosphate-dependent Ca2+ signaling in cat atrial excitation-­contraction coupling and arrhythmias. J Physiol. 2004;555:607–15.

    Article  PubMed  CAS  Google Scholar 

  24. Newton AC, Johnson JE. Protein kinase C: a paradigm for regulation of protein function by two membrane-targeting modules. Biochim Biophys Acta. 1998;1376:155–72.

    PubMed  CAS  Google Scholar 

  25. Malhotra A, Kang BP, Opawumi D, et al. Molecular biology of protein kinase C signaling in cardiac myocytes. Mol Cell Biochem. 2001;225:97–107.

    Article  PubMed  CAS  Google Scholar 

  26. Kamp TJ, Hell JW. Regulation of cardiac L-type calcium channels by protein kinase A and protein kinase C. Circ Res. 2000;87:1095–102.

    PubMed  CAS  Google Scholar 

  27. Churchill E, Budas G, Vallentin A, et al. PKC isozymes in chronic cardiac disease: possible therapeutic targets? Annu Rev Pharmacol Toxicol. 2008;48:569–99.

    Article  PubMed  CAS  Google Scholar 

  28. Dorn 2nd GW, Force T. Protein kinase cascades in the regulation of cardiac hypertrophy. J Clin Invest. 2005;115:527–37.

    PubMed  CAS  Google Scholar 

  29. Sabri A, Steinberg SF. Protein kinase C isoform-selective signals that lead to cardiac hypertrophy and the progression of heart failure. Mol Cell Biochem. 2003;251:97–101.

    Article  PubMed  CAS  Google Scholar 

  30. Hodgkin MN, Pettitt TR, Martin A, et al. Diacylglycerols and phosphatidates: which molecular species are intracellular messengers? Trends Biochem Sci. 1998;23:200–4.

    Article  PubMed  CAS  Google Scholar 

  31. Pettitt TR, Martin A, Horton T, et al. Diacylglycerol and phosphatidate generated by phospholipases C and D, respectively, have distinct fatty acid compositions and functions. Phospholipase D-derived diacylglycerol does not activate protein kinase C in porcine aortic endothelial cells. J Biol Chem. 1997;272:17354–9.

    Article  PubMed  CAS  Google Scholar 

  32. Rebecchi MJ, Pentyala SN. Structure, function, and control of phosphoinositide-specific phospholipase C. Physiol Rev. 2000;80:1291–335.

    PubMed  CAS  Google Scholar 

  33. Song C, Hu CD, Masago M, et al. Regulation of a novel human phospholipase C, PLCε, through membrane targeting by Ras. J Biol Chem. 2001;276:2752–7.

    Article  PubMed  CAS  Google Scholar 

  34. Saunders CM, Larman MG, Parrington J, et al. PLC ζ: a sperm-specific trigger of Ca2+ oscillations in eggs and embryo development. Development. 2002;129:3533–44.

    PubMed  CAS  Google Scholar 

  35. Wing MR, Bourdon DM, Harden TK. PLC-ε: a shared effector protein in Ras-, Rho-, and G αβγ-mediated signaling. Mol Interv. 2003;3:273–80.

    Article  PubMed  CAS  Google Scholar 

  36. Hwang JI, Oh YS, Shin KJ, et al. Molecular cloning and characterization of a novel phospholipase C, PLC-η. Biochem J. 2005;389:181–6.

    Article  PubMed  CAS  Google Scholar 

  37. Tappia PS, Liu S-Y, Shatadal S, et al. Changes in sarcolemmal PLC isoenzymes in postinfarct congestive heart failure: partial correction by imidapril. Am J Physiol. 1999;277:H40–9.

    PubMed  CAS  Google Scholar 

  38. Wolf RA. Association of phospholipase C-δ with a highly enriched preparation of canine sarcolemma. Am J Physiol. 1992;263:C1021–8.

    PubMed  CAS  Google Scholar 

  39. Wang H, Oestreich EA, Maekawa N, et al. Phospholipase C ε modulates β-adrenergic receptor-dependent cardiac contraction and inhibits cardiac hypertrophy. Circ Res. 2005;97:1305–13.

    Article  PubMed  CAS  Google Scholar 

  40. Asemu G, Dhalla NS, Tappia PS. Inhibition of PLC improves postischemic recovery in isolated rat heart. Am J Physiol Heart Circ Physiol. 2004;287:H2598–605.

    Article  PubMed  CAS  Google Scholar 

  41. Kawaguchi H, Sano H, Iizuka K, et al. Phos­phati­dylinositol metabolism in hypertrophic rat heart. Circ Res. 1993;72:966–72.

    PubMed  CAS  Google Scholar 

  42. Shoki M, Kawaguchi H, Okamoto H, et al. Phos­phatidylinositol and inositolphosphatide metabolism in hypertrophied rat heart. Jpn Circ J. 1992;56:142–7.

    Article  PubMed  CAS  Google Scholar 

  43. Sakata Y. Tissue factors contributing to cardiac hypertrophy in cardiomyopathic hamsters (BIO14.6): involvement of transforming growth factor-β1 and tissue renin-angiotensin system in the progression of cardiac hypertrophy. Hokkaido Igaku Zasshi. 1993;68:18–28.

    PubMed  CAS  Google Scholar 

  44. Dent MR, Dhalla NS, Tappia PS. Phospholipase C gene expression, protein content and activities in cardiac hypertrophy and heart failure due to volume overload. Am J Physiol Heart Circ Physiol. 2004;282:H719–27.

    Article  Google Scholar 

  45. Dent MR, Aroutiounova N, Dhalla NS, et al. Losartan attenuates phospholipase C isozyme gene expression in hypertrophied hearts due to volume overload. J Cell Mol Med. 2006;10:470–9.

    Article  PubMed  CAS  Google Scholar 

  46. Katan M. Families of phosphoinositide-specific phospholipase C: structure and function. Biochim Biophys Acta. 1998;1436:5–17.

    PubMed  CAS  Google Scholar 

  47. Jalili T, Takeishi Y, Song G, et al. PKC translocation without changes in Gαq and PLC-β protein abundance in cardiac hypertrophy and failure. Am J Physiol. 1999;277:H2298–304.

    PubMed  CAS  Google Scholar 

  48. Giles TD, Sander GE, Thomas MG, et al. α-adrenergic mechanisms in the pathophysiology of left ventricular heart failure-An analysis of their role in systolic and diastolic dysfunction. J Mol Cell Cardiol. 1986;18:33–43.

    Article  PubMed  CAS  Google Scholar 

  49. Prasad K, O’Neil CL, Bharadwaj B. Effect of ­prolonged prazosin treatment on hemodynamic and biochemical changes in the dog heart due to chronic pressure overload. Jpn Heart J. 1984;25:461–76.

    Article  PubMed  CAS  Google Scholar 

  50. Motz W, Klepzig M, Strauer BE. Regression of cardiac hypertrophy: experimental and clinical results. J Cardiovasc Pharmacol. 1987;10:S148–52.

    PubMed  Google Scholar 

  51. Zakynthinos E, Pierrutsakos CH, Daniil Z, et al. Losartan controlled blood pressure and reduced left ventricular hypertrophy but did not alter arrhythmias in hypertensive men with preserved systolic function. Angiology. 2005;56:439–49.

    Article  PubMed  CAS  Google Scholar 

  52. Kanno Y, Kaneko K, Kaneko M, et al. Angiotensin receptor antagonist regresses left ventricular hypertrophy associated with diabetic nephropathy in dialysis patients. J Cardiovasc Pharmacol. 2004;43:380–6.

    Article  PubMed  CAS  Google Scholar 

  53. Ruzicka M, Yuan B, Leenen FH. Effects of enalapril versus losartan on regression of volume overload-induced cardiac hypertrophy in rats. Circulation. 2004;90:484–91.

    Google Scholar 

  54. Rothermund L, Vetter R, Dieterich M, et al. Endothelin-A receptor blockade prevents left ventricular hypertrophy and dysfunction in salt-sensitive experimental hypertension. Circulation. 2002;106:2305–8.

    Article  PubMed  CAS  Google Scholar 

  55. Yamamoto K, Masuyama T, Sakata Y, et al. Prevention of diastolic heart failure by endothelin type A receptor antagonist through inhibition of ventricular structural remodeling in hypertensive heart. J Hypertens. 2002;20:753–61.

    Article  PubMed  Google Scholar 

  56. Lund AK, Goens MB, Nunez BA, et al. Characterizing the role of endothelin-1 in the progression of cardiac hypertrophy in aryl hydrocarbon receptor (AhR) null mice. Toxicol Appl Pharmacol. 2006;212:127–35.

    Article  PubMed  CAS  Google Scholar 

  57. Bai H, Wu LL, Xing DQ, et al. Angiotensin II induced upregulation of Gαq/11, phospholipase C β3 and extracellular signal-regulated kinase 1/2 via angiotensin II type 1 receptor. Chin Med J. 2004;117:88–93.

    PubMed  CAS  Google Scholar 

  58. Lamers JM, Eskildsen-Helmond YE, Resink AM, et al. Endothelin-1-induced phospholipase C-β and D and protein kinase C isoenzyme in signaling leading to hypertrophy in rat cardiomyocytes. J Cardiovasc Pharmacol. 1995;26:S100–3.

    PubMed  CAS  Google Scholar 

  59. Schnabel P, Mies F, Nohr T, et al. Differential regulation of phospholipase C-β isozymes in cardiomyocyte hypertrophy. Biochem Biophys Res Commun. 2000;275:1–6.

    Article  PubMed  CAS  Google Scholar 

  60. Otaegui D, Querejeta R, Arrieta A, et al. Phospholipase C β4 isozyme is expressed in human, rat, and murine heart left ventricles and in HL-1 cardiomyocytes. Mol Cell Biochem. 2010;337:167–73.

    Article  PubMed  CAS  Google Scholar 

  61. Nagata S. Apoptosis by death factor. Cell. 1997;88:355–65.

    Article  PubMed  CAS  Google Scholar 

  62. Badorff C, Ruetten H, Mueller S, et al. Fas receptor signaling inhibits glycogen synthase kinase 3 β and induces cardiac hypertrophy following pressure overload. J Clin Invest. 2002;109:373–81.

    PubMed  CAS  Google Scholar 

  63. Barac YD, Zeevi-Levin N, Yaniv G, et al. The 1,4,5-inositol trisphosphate pathway is a key component in Fas-mediated hypertrophy in neonatal rat ventricular myocytes. Cardiovasc Res. 2005;68:75–86.

    Article  PubMed  CAS  Google Scholar 

  64. Ruwhof C, van Wamel JT, Noordzij LA, et al. Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal cardiomyocytes. Cell Calcium. 2001;29:73–83.

    Article  PubMed  CAS  Google Scholar 

  65. D’Angelo DD, Sakata Y, Lorenz JN, et al. Transgenic Gαq overexpression induces cardiac contractile failure in mice. Proc Natl Acad Sci USA. 1997;94:8121–6.

    Article  PubMed  Google Scholar 

  66. Sakata Y, Hoit BD, Liggett SB, et al. Decompensation of pressure-overload hypertrophy in Gαq-overexpressing mice. Circulation. 1998;97:1488–95.

    PubMed  CAS  Google Scholar 

  67. Adams JW, Sakata Y, Davis MG, et al. Enhanced Gαq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proc Natl Acad Sci USA. 1998;95:10140–5.

    Article  PubMed  CAS  Google Scholar 

  68. Sussman MA, Welch S, Walker A, et al. Altered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1. J Clin Invest. 2000;105:875–86.

    Article  PubMed  CAS  Google Scholar 

  69. Paradis P, Dali-Youcef N, Paradis FW, et al. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci USA. 2000;97:931–6.

    Article  PubMed  CAS  Google Scholar 

  70. Mende U, Kagen A, Cohen A, et al. Transient cardiac expression of constitutively active Gαq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways. Proc Natl Acad Sci USA. 1998;95:13893–8.

    Article  PubMed  CAS  Google Scholar 

  71. Mende U, Kagen A, Meister M, et al. Signal transduction in atria and ventricles of mice with transient cardiac expression of activated G protein αq. Circ Res. 1999;85:1085–91.

    PubMed  CAS  Google Scholar 

  72. Mende U, Semsarian C, Martins DC, et al. Dilated cardiomyopathy in two transgenic mouse lines expressing activated G protein αq: lack of correlation between phospholipase C activation and the phenotype. J Mol Cell Cardiol. 2001;33:1477–91.

    Article  PubMed  CAS  Google Scholar 

  73. Hollinger S, Hepler JR. Cellular regulation of RGS proteins: modulators and integrators of G protein signaling. Pharmacol Rev. 2002;54:527–59.

    Article  PubMed  CAS  Google Scholar 

  74. Anger T, Zhang W, Mende U. Differential contribution of GTPase activation and effector antagonism to the inhibitory effect of RGS proteins on Gq-mediated signaling in vivo. J Biol Chem. 2004;279:3906–15.

    Article  PubMed  CAS  Google Scholar 

  75. Zhang W, Anger T, Su J, et al. Selective loss of fine tuning of Gq/11 signaling by RGS2 protein exacerbates cardiomyocyte hypertrophy. J Biol Chem. 2006;281:5811–20.

    Article  PubMed  CAS  Google Scholar 

  76. Lin F, Owens WA, Chen S, et al. Targeted α1B-adrenergic receptor overexpression induces enhanced cardiac contractility but not hypertrophy. Circ Res. 2001;89:343–50.

    Article  PubMed  CAS  Google Scholar 

  77. Milano CA, Dolber PC, Rockman HA, et al. Myocardial expression of a constitutively active 1β-adrenergic receptor in transgenic mice induces cardiac hypertrophy. Proc Natl Acad Sci USA. 1994;91:10109–13.

    Article  PubMed  CAS  Google Scholar 

  78. Heemskerk JWM, Farndale RW, Sage SO. Effects of U73122 and U73343 on human platelet calcium ­signalling and protein tyrosine phosphorylation. Biochim Biophys Acta. 1997;1355:81–8.

    Article  PubMed  CAS  Google Scholar 

  79. Jin W, Lo TM, Loh HH, et al. U73122 inhibits phospholipase C-dependent calcium mobilization in ­neuronal cells. Brain Res. 1994;642:237–43.

    Article  PubMed  CAS  Google Scholar 

  80. Mogami H, Mills CL, Gallagher DV. Phospholipase C inhibitor, U73122, releases intracellular Ca2+, potentiates Ins(1,4,5)P-3-mediated Ca2+ release and directly activates inn channels in mouse pancreatic acinar cells. Biochem J. 1997;324:645–51.

    PubMed  CAS  Google Scholar 

  81. Muto Y, Nagao T, Urushidani T. The putative phospholipase C inhibitor U73122 and its negative control, U73343, elicit unexpected effects on the rabbit parietal cell. J Pharmacol Exp Ther. 1997;282:1379–88.

    PubMed  CAS  Google Scholar 

  82. Berven LA, Barritt GJ. Evidence obtained using single hepatocytes for inhibition by the phospholipase C inhibitor U73122 of store-operated Ca2+ inflow. Biochem Pharmacol. 1995;49:1373–9.

    Article  PubMed  CAS  Google Scholar 

  83. Arthur JF, Matkovich SJ, Mitchell CJ, et al. Evidence for selective coupling of α1-adrenergic receptors to phospholipase C-β1 in rat neonatal cardiomyocytes. J Biol Chem. 2001;276:37341–6.

    Article  PubMed  CAS  Google Scholar 

  84. Grubb DR, Vasilevski O, Huynh H, et al. The extreme C-terminal region of phospholipase C β1 determines subcellular localization and function; the “b” splice variant mediates α1- adrenergic receptor responses in cardiomyocytes. FASEB J. 2008;22:2768–74.

    Article  PubMed  CAS  Google Scholar 

  85. Morris JB, Huynh H, Vasilevski O, et al. α1-Adrenergic receptor signaling is localized to caveolae in neonatal rat cardiomyocytes. J Mol Cell Cardiol. 2006;41:117–25.

    Article  CAS  Google Scholar 

  86. Filtz TM, Grubb DR, McLeod-Dryden TJ, et al. Gq-initiated cardiomyocyte hypertrophy is mediated by phospholipase Cβ1b. FASEB J. 2009;23:3564–70.

    Article  PubMed  CAS  Google Scholar 

  87. Barka T, van der Noen H, Shaw PA. Proto-oncogene fos (c-fos) expression in the heart. Oncogene. 1987;1:439–43.

    PubMed  CAS  Google Scholar 

  88. Hannan RD, West AK. Adrenergic agents, but not triiodo-L-thyronine induce c-fos and c-myc expression in the rat heart. Basic Res Cardiol. 1991;86:154–64.

    Article  PubMed  CAS  Google Scholar 

  89. Iwaki K, Sukhatme VP, Shubeita HE, et al. α- and β-adrenergic stimulation induces distinct patterns of immediate early gene expression in neonatal rat myocardial cells. fos/jun expression is associated with sarcomere assembly; Egr-1 induction is primarily an α1-mediated response. J Biol Chem. 1990;265:13809–17.

    PubMed  CAS  Google Scholar 

  90. Komuro I, Kaida T, Shibazaki Y, et al. Stretching cardiac myocytes stimulates protooncogene expression. J Biol Chem. 1990;265:3595–8.

    PubMed  CAS  Google Scholar 

  91. Hefti MA, Harder BA, Eppenberger HM, et al. Signaling pathways in cardiac myocyte hypertrophy. J Mol Cell Cardiol. 1997;29:2873–92.

    Article  PubMed  CAS  Google Scholar 

  92. Chiu R, Boyle WJ, Meek J, et al. The c-Fos protein interacts with c-Jun/AP-1 to stimulate transcription of AP-1 responsive genes. Cell. 1988;54:541–52.

    Article  PubMed  CAS  Google Scholar 

  93. Lijnen P, Petrov V. Antagonism of the re1nin-angiotensin system, hypertrophy and gene expression in cardiac myocytes. Methods Fund Exp Clin Pharmacol. 1999;21:363–74.

    Article  CAS  Google Scholar 

  94. Omura T, Yoshiyama M, Yoshida K, et al. Dominant negative mutant of c-Jun inhibits cardiomyocyte hypertrophy induced by endothelin 1 and phenylephrine. Hypertension. 2002;39:81–6.

    Article  PubMed  CAS  Google Scholar 

  95. Singal T, Dhalla NS, Tappia PS. Reciprocal regulation of transcription factors and PLC isozyme gene expression in adult cardiomyocytes. J Cell Mol Med. 2010;14:1824–35.

    Article  PubMed  CAS  Google Scholar 

  96. Singal T, Dhalla NS, Tappia PS. Regulation of c-Fos and c-Jun gene expression by phospholipase C activity in adult cardiomyocytes. Mol Cell Biochem. 2009;327:229–39.

    Article  PubMed  CAS  Google Scholar 

  97. Dhalla NS, Xu Y-J, Sheu S-S, et al. Phosphatidic acid: a potential signal transducer for cardiac hypertrophy. J Mol Cell Cardiol. 1997;29:2865–71.

    Article  PubMed  CAS  Google Scholar 

  98. Small K, Feng JF, Lorenz J, et al. Cardiac specific overexpression of transglutaminase II (Gh) results in a unique hypertrophy phenotype independent of phospholipase C activation. J Biol Chem. 1999;23:21291–6.

    Article  Google Scholar 

  99. Tappia PS, Yu CH, Di Nardo P, et al. Depressed responsiveness of phospholipase C isoenzymes to phosphatidic acid in congestive heart failure. J Mol Cell Cardiol. 2001;33:431–40.

    Article  PubMed  CAS  Google Scholar 

  100. Henry RA, Boyce SY, Kurz T, et al. Stimulation and binding of myocardial phospholipase C by phosphatidic acid. Am J Physiol. 1995;269:C349–58.

    PubMed  CAS  Google Scholar 

  101. Tappia PS, Singal T. Regulation of phospholipase C in cardiac hypertrophy. Clin Lipidol. 2009;4:79–90.

    Article  CAS  Google Scholar 

  102. Peivandi AA, Huhn A, Lehr HA, et al. Upregulation of phospholipase D expression and activation in ventricular pressure-overload hypertrophy. J Pharmacol Sci. 2005;98:244–54.

    Article  PubMed  CAS  Google Scholar 

  103. Eskildsen-Helmond YE, Bezstarosti K, Dekkers DH, et al. Cross-talk between receptor-mediated phospholipase C-β and D via protein kinase C as intracellular signal possibly leading to hypertrophy in serum-free cultured cardiomyocytes. J Mol Cell Cardiol. 1997;29:2545–59.

    Article  PubMed  CAS  Google Scholar 

  104. Murthy SN, Chung PH, Lin L, et al. Activation of phospholipase Cε by free fatty acids and cross talk with phospholipase D and phospholipase A2. Biochemistry. 2006;45:10987–97.

    Article  PubMed  CAS  Google Scholar 

  105. Liu SY, Tappia PS, Dai J, et al. Phospholipase A2-mediated activation of phospholipase D in rat heart sarcolemma. J Mol Cell Cardiol. 1998;30:1203–14.

    Article  PubMed  CAS  Google Scholar 

  106. Strauer BE, Bayer F, Brecht HM, et al. The influence of sympathetic nervous activity on regression of cardiac hypertrophy. J Hypertens. 1985;3:S39–44.

    Article  CAS  Google Scholar 

  107. Strauer BE. Progression and regression of heart hypertrophy in arterial hypertension: pathophysiology and clinical aspects. Z Kardiol. 1995;74:171–8.

    Google Scholar 

  108. Strauer BE. Regression of myocardial and coronary vascular hypertrophy in hypertensive heart disease. J Cardiovasc Pharmacol. 1988;12:S45–54.

    Article  PubMed  Google Scholar 

Download references

Acknowledgements

The work reported in this article was supported by the Heart and Stroke Foundation of Manitoba. Infrastructural support was provided by the St. Boniface Hospital Research Foundation.

Author information

Authors and Affiliations

  1. Asper Clinical Research Institute, St. Boniface Hospital Research and Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada

    Paramjit S. Tappia

Authors
  1. Paramjit S. Tappia
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Paramjit S. Tappia .

Editor information

Editors and Affiliations

  1. St. Boniface General Hospital, Research Centre, Institute of Cardiovascular Sciences, Tache Avenue 351, Winnipeg, R2H 2A6, Manitoba, Canada

    Naranjan S. Dhalla

  2. Jikei University School of Medicine, Shibuya-ku, Ebisu 3-31-6, Tokyo, 150-0013, Japan

    Makoto Nagano

  3. Czech Republic, Institute of Physiology, Academy of Sciences of the, Videnska 1083, Prague, 142 20, Czech Republic

    Bohuslav Ostadal

Rights and permissions

Reprints and permissions

Copyright information

© 2011 Springer Science+Business Media, LLC

About this chapter

Cite this chapter

Tappia, P.S. (2011). Mechanisms for the Regulation of Phospholipase C Gene Expression in Cardiac Hypertrophy. In: Dhalla, N., Nagano, M., Ostadal, B. (eds) Molecular Defects in Cardiovascular Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-7130-2_11

Download citation

  • DOI: https://doi.org/10.1007/978-1-4419-7130-2_11

  • Published:

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4419-7129-6

  • Online ISBN: 978-1-4419-7130-2

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation