Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1

PLoS ONE

Volumn 7, Issue 5, 2012, Pages

  Xiao, Jinfeng ^a,b   Jiang, Hong ^a,b   Zhang, Rui ^a,b   Fan, Guangpu ^c   Zhang, Yan ^a,b   Jiang, Dingsheng ^a,b   Li, Hongliang ^a,b  

^a RENMIN HOSPITAL OF WUHAN UNIVERSITY   (China)

^b WUHAN UNIVERSITY   (China)

^c HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

EPIDERMAL GROWTH FACTOR LATROPHILIN AND SEVEN TRANSMEMBRANE DOMAIN CONTAINING PROTEIN 1; MEMBRANE PROTEIN; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG; ELTD1 PROTEIN, HUMAN; G PROTEIN COUPLED RECEPTOR; PRIMER DNA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DISEASE EXACERBATION; ELTD1 GENE; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; GENE; GENE DELETION; GENE EXPRESSION REGULATION; GENE FUNCTION; GENE INACTIVATION; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; HEART VENTRICLE REMODELING; HUMAN; HUMAN TISSUE; INTRACELLULAR SIGNALING; MALE; MOUSE; NONHUMAN; PROTEIN EXPRESSION; PROTEIN FUNCTION; WILD TYPE; ANIMAL; C57BL MOUSE; CARDIOMEGALY; CASE CONTROL STUDY; FIBROSIS; GENETICS; HEART FAILURE; HEART MUSCLE CELL; METABOLISM; MOUSE MUTANT; NUCLEOTIDE SEQUENCE; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; SIGNAL TRANSDUCTION;

MUS;

ANIMALS; BASE SEQUENCE; CARDIOMEGALY; CASE-CONTROL STUDIES; DNA PRIMERS; FIBROSIS; HEART FAILURE; HUMANS; MALE; MAP KINASE SIGNALING SYSTEM; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCYTES, CARDIAC; PROTO-ONCOGENE PROTEINS C-AKT; RECEPTORS, G-PROTEIN-COUPLED;

EID: 84860991788     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0035779     Document Type: Article

References (34)

1. Bernardo BC, Weeks KL, Pretorius L, McMullen JR, (2010) Molecular distinction between physiological and pathological cardiac hypertrophy: Experimental findings and therapeutic strategies. Pharmacol Ther 128: 191-227.
2. Belmonte SL, Blaxall BC, (2011) G protein coupled receptor kinases as therapeutic targets in cardiovascular disease. Circ Res 109: 309-319.
3. Zhang P, Mende U, (2011) Regulators of G-protein signaling in the heart and their potential as therapeutic targets. Circ Res 109: 320-333.
4. Nechiporuk T, Urness LD, Keating MT, (2001) ETL, a novel seven-transmembrane receptor that is developmentally regulated in the heart. ETL is a member of the secretin family and belongs to the epidermal growth factor-seven-transmembrane subfamily. J Biol Chem 276: 4150-4157.
5. Luttrell LM, van Biesen T, Hawes BE, Koch WJ, Krueger KM, et al. (1997) G-protein-coupled receptors and their regulation: activation of the MAP kinase signaling pathway by G-protein-coupled receptors. Adv Second Messenger Phospho protein Res 31: 263-277.
6. Pak Y, O'Dowd BF, Wang JB, George SR, (1999) Agonist-induced, G Protein-dependent and-independent down-regulation of the μ Opioid Receptor. J Biol Chem 274: 27610-27616.
7. Li H, He C, Feng J, Zhang Y, Tang Q, et al. (2010) Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload. Proc Natl Acad Sci U S A 107 (31): 13818-138238.
8. Creemers EE, Pinto YM, (2011) Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart. Cardiovasc Res 89: 265-272.
9. Proud CG, (2004) Ras, PI3-kinase and mTOR signaling in cardiac hypertrophy. Cardiovasc Res 63: 403-413.
10. Rose BA, Force T, Wang Y, (2010) Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. Physiol Rev 90: 1507-1546.
11. Kubo T, Gimeno JR, Bahl A, Steffensen U, Steffensen M, et al. (2007) Prevalence, clinical significance, and genetic basis of hypertrophic cardiomyopathy with restrictive phenotype. J Am Coll Cardiol49: 2419-2426.
12. Spirito P, Seidman CE, McKenna WJ, Maron BJ, (1997) The management of hypertrophic cardiomyopathy. N Engl J Med 336: 775-785.
13. Biagini E, Coccolo F, Ferlito M, Perugini E, Rocchi G, et al. (2005) Dilated-hypokinetic evolution of hypertrophic cardiomyopathy: prevalence, incidence, risk factors, and prognostic implications in pediatric and adult patients. J Am Coll Cardiol 46: 1543-1550.
14. Inesi G, Prasad AM, Pilankatta R, (2008) The Ca2+ ATPase of cardiac sarcoplasmic reticulum: Physiological role and relevance to diseases. Biochem Biophys Res Commun 369: 182-187.
15. Brooks WW, Conrad CH, (2000) Myocardial fibrosis in transforming growth factor β1 heterozygous mice.J Mol Cell Cardiol 32: 187-195.
16. Rosenkranz S, Flesch M, Amann K, Haeuseler C, Kilter H, et al. (2002) Alterations of β-adrenergic signaling and cardiac hypertrophy in transgenic mice overexpressing TGF-β1. Am J Physiol Heart Circ Physiol 283: H1253-H1262.
17. Panek AN, Posch MG, Alenina N, Ghadge SK, Erdmann B, et al. (2009) Connective tissue growth factor overexpression in cardiomyocytes promotes cardiac hypertrophy and protection against pressure overload. PLoS One 4: e6743.
18. Berk BC, Fujiwara K, Lehoux S, (2007) ECM remodeling in hypertensive heart disease. J Clin Invest 117: 568-575.
19. Purcell NH, Wilkins BJ, York A, Saba-El-Leil MK, Meloche S, et al. (2007) Genetic inhibition of cardiac ERK1/2 promotes stress-induced apoptosis and heart failure but has no effect on hypertrophy in vivo. Proc Natl Acad Sci U S A 104: 14074-14079.
20. Rose BA, Force T, Wang Y, (2010) Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. Physiol Rev 90: 1507-1546.
21. Xiao JF, Moon M, Yan L, Nian M, Zhang Y, et al. (2012) Cellular FLICE-inhibitory protein protects against cardiac remodelling after myocardial infarction. Basic Res Cardiol 107: 1-21.
22. Robbins DJ, Zhen E, Owaki H, Vanderbilt CA, Ebert D, et al. (1993) Regulation and properties of extracellular signal-regulated protein kinases 1 and 2 in vitro. J Biol Chem 268: 5097-5106.
23. Lorenz K, Schmitt JP, Schmitteckert EM, Lohse MJ, (2009) A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy. Nat Med 15: 75-83.
24. Karin M, (1996) The regulation of AP-1 activity by mitogen-activated protein kinases. Philos Trans R Soc Lond B Biol Sci 351: 127-134.
25. Liu W, Zi M, Jin J, Prehar S, Oceandy D, et al. (2009) Cardiac-specific deletion of MKK4 reveals its role in pathological hypertrophic remodeling but not in physiological cardiac growth. Circ Res.104: 905-914.
26. Choukroun G, Hajjar R, Fry S, Monte Fd, Haq S, et al. (1999) Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH2-terminal kinases. J Clin Invest 104: 391-399.
27. Kim S, Iwao H, (1999) Activation of mitogen-activated protein kinases in cardiovascular hypertrophy and remodeling. Jpn J Pharmacol 80: 97-102.
28. Liao P, Georgakopoulos D, Kovacs A, Zheng M, Lerner D, et al. (2001) The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy.Proc Natl Acad Sci U S A 98: 12283-12288.
29. Zhang S, Weinheimer C, Courtois M, Kovacs A, Zhang C, et al. (2003) The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis. J Clin Invest 111: 833-841.
30. Braz JC, Bueno OF, Liang Q, Wilkins BJ, Dai YS, et al. (2003) Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling. J Clin Invest 111: 1475-1486.
31. Sari FR, Widyantoro B, Thandavarayan RA, Harima M, Lakshmanan AP, et al. (2011) Attenuation of CHOP-mediated myocardial apoptosis in pressure-overloaded dominant negative p38α mitogen-activated protein kinase mice. Cell Physiol Biochem 27: 487-496.
32. Cai W-F, Zhang X-W, Yan H-M, Ma Y-G, Wang X-X, et al. (2010) Intracellular or extracellular heat shock protein 70 differentially regulates cardiac remodelling in pressure overload mice. Cardiovasc Res 88: 140-149.
33. Dingar D, Merlen C, Grandy S, Gillis M-A, Villeneuve LR, et al. (2010) Effect of pressure overload-induced hypertrophy on the expression and localization of p38 MAP kinase isoforms in the mouse heart. Cell Signal 22: 1634-1644.
34. Matsui T, Li L, Wu J, Cook S, Nagoshi T, et al. (2002) Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. J Biol Chem 277: 22896-22901.