Van Eyk, Dunn - Proteomic and Genomic Analysis of Cardiovascular Disease - 2003 (522919), страница 21
Текст из файла (страница 21)
Large-scale DNA sequencing and theuse of microarray technology have provided biomedical researchers with powerfultools to handle the vast database of the Human Genome Project. Structural biol-57583 Heart Failure: A Genomics Approachogy and computational technology will further refine the structure predictionmethod and help decipher the complexity of sequence-structure-function in biological science. With the expanding database of newly discovered novel genes andfunctional annotations, therapeutic modalities aimed at specific molecular targetsmay be more effective and closer than previously imagined.3.5AcknowledgementsI would especially like to thank Isolde Prince for her help in preparing this manuscript.
I would also like to thank David Barrans, Adam Dempsey, Jim Hwang, andDimitri Stamatiou for their comments and suggestions.3.6References123456789Towbin, J. A., Bowles, N. E. The failingheart. Nature. 2002. 415, 227–233.Miller, L. W., Missov, E. D. Epidemiology of heart failure. Cardiology Clinics2001. 19, 547–555.Ho, K. K. L., Anderson, K. M., Kannel,W. B., Grossman,W., Levy, D., et al. Survival after the onset of congestive heartfailure in Framingham Heart Study subjects. Circulation 1993. 88, 107–115.Nohria, A., Lewis, E., Stevenson, L.Medical Management of advanced heartfailure.
J.A.M.A. 2002. 287, 628–640.Karon, B. L. Diagnosis and outpatientmanagement of congestive heart failure.Mayo Clinic Proceedings. 1995. 70, 1080–1085.Francis, G. S. Pathophysiology ofchronic heart failure. Am. J. Med. 2001.110(7A): 37S–46S.Marban, E. Cardiac channelopathies. Nature. 2002. 415, 213–218.Cohn, J. N., Ferrari, R., Sharpe, N.Cardiac remodeling concepts and clinicalimplications: a consensus paper from aninternational forum on cardiac remodelling. J. Am.
Coll. Cardiol. 2000. 35, 569–582.Hwang, J. J., Dzau, V. J., Liew, C. C.Genomics and the pathophysiology of1011121314heart failure. Current Cardiol. Rep. 2001.3, 198–207.Ducharme, A., Frantz, S., Aikawa, M.,Rabkin, E., et al. Targeted deletion ofmatrix metalloproteinase – 9 attenuatesleft ventricular enlargement and collagenaccumulation after experimental myocardial infarction J. Clin. Invest. 2000. 106,55–62.Kim, H. E., Dalal, S. S., Young, E., Legato, M. J., et al. Disruption of the myocardial extracellular matrix leads to cardiacdysfunction.
J. Clin. Invest. 2000. 106,857–866.Givertz, M. M., Colucci, W. S. New targets for heart-failure therapy: endothelin,inflammatory cytokines and oxidativestress. Lancet 1998. 352 Suppl. 1, 34–38.Dieterich, S., Bieligk, U., Beulich, K.,Hasenfuss, G., et al. Gene expression ofantioxidative enzymes in the humanheart: increased expression of catalase inthe end-stage failing heart. Circulation2000. 101, 33–39.Siwik, D. A., Tzortzis, J.
D., Pimental,D. R., Chang, D. L., et al. Inhibition ofcopper-zinc superoxidase dismutase induces cell growth, hypertrophic phenotype and apoptosis in neonatal rat cardi-3.6 References151617181920212223242526ac myocytes in vitro. Circ. Res. 1999. 85,147–153.De Jong, J.
W., Schoemaker, R. G., DeJonge, R., Bernocchi, P., et al. Enhanced expression and activity ofxanthine oxidoreductase in the failingheart. J. Mol. Cell. Cardiol. 2000. 32,2083–2089.Sack, M. N., Kelly, D. P. The energy substrate switch during development ofheart failure: gene regulatory mechanisms. Int. J. Mol. Med. 1998. 1, 17–24.Venter, J. C., Adams, M. D., Myers, E.
W.,Li, P. W., et al. The sequence of the humangenome. Science 2001. 291, 1304–1351.International Human Genome Sequencing Consortium. Initial sequencing and analysis of the human genome.Nature 2001. 409, 860–921.Chien, K. R. Genomic circuits and theintegrative biology of cardiac diseases.Nature 2000. 407, 227–232.Pratt, R. E., Dzau, V. J.
Genomics andhypertension: concepts, potentials andopportunities. Hypertension 1999. 33 part2, 238–247.Dempsey, A. A., Ton, C., Liew, C. C. Acardiovascular EST repertoire: progressand promise for understanding cardiovascular disease. Mol. Med. Today 2000.6, 231–237.Liew, C. C. A human heart cDNA librarythe development of an efficient and simplemethod for automated DNA sequencing. J.Mol. Cell. Cardiol. 1993. 25, 891–894.Ton, C., Hwang, D.
M., Dempsey A. A.,Tang, H. C., et al. Identification, characterization and mapping of expressed sequence tags from an embryonic zebrafishheart cDNA library. Genome Research2000. 10, 1915–1927.Hwang, D. M., Dempsey, A. A., Lee, C. Y.,Liew, C. C. Identification of differentiallyexpressed genes in cardiac hypertrophyby analysis of expressed sequence tags.Genomics 2000.
66, 1–14.Collins, F. S., Patrinos, A., Jordan, E.,Chakravarti A., et al. New goals for theUS Human Genome Project: 1998–2003.Science 1998. 282, 682–689.Dempsey, A. A., Dzau, V. J., Liew, C. C.Cardiovascular genomics: estimating thetotal number of genes expressed in the27282930313233343536human cardiovascular system. J. Mol.Cell. Cardiol. 2001. 33, 1879–1886.Alizadeh, A. A., Eisen, M.
B., Davis,R. E., Ma, C., et al. Distinct types of diffuse large B-cell lymphoma identified bygene expression profiling. Nature 2000.403, 503–511.Gasch, A. P., Spellman, P. T., Kao, C. M.,Carmel-Harel, O., et al. Genomic expression programs in the response ofyeast cells to environmental changes.Mol. Biol. Cell 2000. 11, 4241–57.Stanton, L.
W., Garrard, L. J., Damm,D., Garrick, B. L. et al. Altered patternsof gene expression in response to myocardial infarction. Circ. Res. 2000. 86,939–945.Friddle, C. L., Koga, T., Rubin, E. M.,Bristow, J. Expression profiling revealsdistinct sets of genes altered during induction and regression of cardiac hypertrophy. P.N.A.S. 2000.
97, 6745–6750.Taylor, L. A., Carthy, C. M., Yang, D., etal. Host gene regulation during coxsackievrus B3 infection in mice: assessmentby microarrays. Circ. Res. 2000 87, 328–334.Adams, L. D., Geary, R. L., McManus, B.,Schwartz, S. M. A comparison of aortaand vena cava medial message expression by cDNA array analysis identifies aset of 68 consistently differentially expressed genes, all in aortic media.
Circ.Res. 2000 87, 623–631.Yang, J., Moravec, C. S., Sussman,M. A., DiPaola, N. R., et al. DecreasedSLIM1 expression and increased gelsolinexpression in failing human hearts measured by high-density oligonucleotide arrays. Circulation 2000. 102, 3046–3052.Barrans, J. D., Stamatiou, D., Liew,C. C. Construction of a human cardiovascular cDNA microarray: portrait of thefailing heart. Biochem. Biophys. Res.Comm. 2001. 280, 964–969.Barrans, J. D., Allen, P. D., Stamatiou,D., Dzau, V. J., Liew, C.
C. Global geneexpression of end-stage dilated cardiomyopathy using a human cardiovascularbased cDNA microarray Am. J. Pathol.2002. (in press).Vikstrom, K. L., Bohlmeyer, T., Factor,S. M., Leinwand, L. A. Hypertrophy,59603 Heart Failure: A Genomics Approach37383940414243444546pathology and molecular markers of cardiac pathogenesis. Circ. Res.
1998. 82,773–778.Towbin, J. A., Bowles, N. E. Genetic abnormalities responsible for dilated cardiomyopathy. Curr. Cardiol. Rep. 2000. 2,475–480.Towbin, J. A. The role of cytoskeletal proteins in cardiomyopathies Curr. Opin.Cell. Biol. 1998. 10, 131–139.Elliott, K., Watkins, H., Redwood,C. S. Altered regulatory properties of human cardiac troponin I mutants thatcause hypertrophic cardomyopathy J.Biol. Chem.
2000. 275, 22069–22074.Kimura, A., Harada, H., Park, J. E.,Nishi, H., et al. Mutations in the cardiactroponin I gene associated with hypertrophic cardiomyopathy Nat. Genet. 1997.16, 379–382.Redwood, C., Lohmann, K., Bing, W.,Esposito, G. M., et al. Investigation of atruncated cardiac troponin T that causesfamilial hypertrophic cardiomyopathy:Ca(2+) regulatory properties of reconstituted thin filaments depend on the ratioof mutant to wild-type protein. Circ. Res.2000. 86, 1146–1152.Geisterfer-Lowrance, A. A., Kass, S.,Tanigawa, G., Vosberg, H. P., et al. Amolecular basis for familial hypertrophiccardiomyopthy: a beta cardiac myosinheavy chain gene missense mutation.Cell 1990. 62, 999–1006.Thierfelder, L., Watkins, H., MacRae,C., Lamas, R., et al.
Alpha-tropomyosinand cardiac troponin T mutations causefamilial hypertrophic cardiomyopathy adisease of the sarcomere. Cell. 1994. 77,701–712.Arber, S., Hunter, J. J., Ross, J. Jr.,Hongo, M., et al. MLP-deficient mice exhibit a disruption of cardiac cytoarchitectural organization, dilated cardiomyopathyand heart failure. Cell. 1997. 88, 393–403.Dalakas, M.
C., Park, K. Y., SeminoMora. C., Lee, H. S., et al. Desmin myopathy a skeletal myopathy with cardiomyopathy caused by mutations in thedesmin gene. N. Engl. J. Med. 2000. 342,770–780.Satoh, M., Takahashi, M., Sakamoto,T., Hiroe, M., et al. Structural analysis of4748495051525354555657the titin gene in hypertrophic cardiomyopathy: identification of an novel diseasegene. Biochem. Biophys. Res.
Commun.1999. 27, 411–417.Olson, T. M., Michels, V. V., Thibodeau, S. N., Tai, Y. S., Keating M. T. Actin mutations in dilated cardiomyopathy,a heritable form of heart failure. Science1998. 280, 750–752.Schonberger, J., Seidman, C. E. Manyroads lead to a broken heart: the geneticsof dilated cardiomyopthy. Am. J. Hum.Genet. 2001. 69, 249–260.Francis, G. S. Changing the remodelingprocess in heart failure: basic mechanisms and laboratory results. Curr.
Opin.Cardiol. 1998. 13, 156–161.Rao, V. U., Spinale, F. G. Controllingmyocardial matrix remodeling: implications for heart failure. Cardiol. Rev. 1999.7, 136–143.McKinsey, T. A., Olson, E. N. Cardiac hypertrophy: sorting out the circuitry Curr.Opin. Genet.