Array Transcription Profiling: Molecular Phenotyping of Rodent Cardiovascular Models
Chapter
First Online:
Abstract
Since its introduction just a few years ago, array transcription profiling (TP) has emerged as a powerful tool for the study of gene expression in cells and tissues, normal and diseased, across biological systems from bacteria to humans. In principle, TP measures expression levels for thousands of genes simultaneously and allows comparisons of these levels across different experimental conditions. Among the important applications of this technology is the molecular phenotyping of rodent genetic models. Gene expression profiling in engineered animals can be used in conjunction with cardiovascular anatomy, histology, and physiology to develop hypotheses regarding the roles of key genes in normal and disease biology. It has the potential to uncover not only individual genes but entire molecular pathways that operate in the cells of the cardiovascular system. In this chapter we will review the fundamentals of array TP, outline basic methodology, and discuss applications with a focus on rodent models of cardiovascular disease.
Keywords
Atrial Natriuretic Factor Transcription Profile Cardiac Phenotype Cardiovascular Physiology Genetically Engineer Mouse
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Preview
Unable to display preview. Download preview PDF.
References
- 1.Schena M, Shalon D, Davis RW, Brown PO. Quantitative monitoring of gene expression patterns with a complementary DNA microarray. Science. 1995;270:467–470.PubMedCrossRefGoogle Scholar
- 2.Schena M, Shalon D, Heller R, Chai A, Brown PO, Davis RW. Parallel human genome analysis: microarray-based expression monitoring of 1000 genes. Proc Nati Acad Sci USA. 1996;93:10614–10619.CrossRefGoogle Scholar
- 3.Ramsay G. DNA chips: state-of-the art. Nat Biotechnol. 1998;16:40–44.PubMedCrossRefGoogle Scholar
- 4.Watson A, Mazumder A, Stewart M, Balasubramanian S. Technology for microarray analysis of gene expression. Curr Opin Biotechnol. 1998;9:609–614.PubMedCrossRefGoogle Scholar
- 5.Zweiger G. Knowledge discovery in gene-expression-microarray data: mining the information output of the genome. Trends Biotechnol. 1999;17:429–436.PubMedCrossRefGoogle Scholar
- 6.Liang P, Pardee AB. Differential display of eukaryotic messenger RNA by means of the polymerase chain reaction. Science. 1992;257:967–971.PubMedCrossRefGoogle Scholar
- 7.Hubank M, Schatz DG. Identifying differences in mRNA expression by representational difference analysis of cDNA. Nucleic Acids Res. 1994;22:5640–5648.PubMedCrossRefGoogle Scholar
- 8.Velculescu VE, Zhang L, Vogelstein B, Kinzler KW. Serial analysis of gene expression. Science. 1995;270:484–487.PubMedCrossRefGoogle Scholar
- 9.Winzeler EA, Schena M, Davis RW. Fluorescence-based expression monitoring using microarrays. Methods Enzymol. 1999;306:3–18.PubMedCrossRefGoogle Scholar
- 10.Lee ML, Kuo FC, Whitmore GA, Sklar J. Importance of replication in microarray gene expression studies: statistical methods and evidence from repetitive cDNA hybridizations. Proc Natl Acad Sci USA. 2000;97:9834–9839.PubMedCrossRefGoogle Scholar
- 11.Redfern CH, Degtyarev MY, Kwa AT, Salomonis N, Cotte N, Nanevicz T, Fidelman N, Desai K, Vranizan K, Lee EK, Coward P, Shah N, Warrington JA, Fishman GI, Bernstein D, Baker AJ, Conklin BR. Conditional expression of a Gi-coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy. Proc Natl Acad Sci USA. 2000;97:4826–4831.PubMedCrossRefGoogle Scholar
- 12.Dansky HM, Charlton SA, Sikes JL, Heath SC, Simantov R, Levin LF, Shu P, Moore KJ, Breslow JL, Smith JD. Genetic background determines the extent of atherosclerosis in ApoE-deficient mice. Arterioscler Thromb Vasc Biol. 1999;19:1960–1968.PubMedCrossRefGoogle Scholar
- 13.McConnell BK, Jones KA, Fatkin D, Arroyo LH, Lee RT, Aristizabal O, Turnbull DH, Georgakopoulos D, Kass D, Bond M, Niimura H, Schoen FJ, Conner D, Fischman DA, Seidman CE, Seidman JG, Fischman DH. Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice. J Clin Invest. 1999;104:1235–1244.PubMedCrossRefGoogle Scholar
- 14.Donovan MJ, Hahn R, Tessarollo L, Hempstead BL. Identification of an essential nonneuronal function of neurotrophin 3 in mammalian cardiac development. Nat Genet. 1996;14:210–213.PubMedCrossRefGoogle Scholar
- 15.Arber S, Hunter JJ, Ross J, Jr., Hongo M, Sansig G, Borg J, Perriard JC, Chien KR, Caroni P. MLP-deficient mice exhibit a disruption of cardiac cytoarchitectural organization, dilated cardiomyopathy, and heart failure. Cell. 1997;88:393–403.PubMedCrossRefGoogle Scholar
- 16.Lyn D, Liu X, Bennett NA, Emmett NL. Gene expression profile in mouse myocardium after ischemia. Physiol Genomics. 2000;2:93–100.PubMedGoogle Scholar
- 17.Sehl PD, Tai JT, Hillan KJ, Brown LA, Goddard A, Yang R, Jin H, Lowe DG. Application of cDNA microarrays in determining molecular phenotype in cardiac growth, development, and response to injury. Circulation. 2000;101:1990–1999.PubMedCrossRefGoogle Scholar
- 18.Stanton LW, Garrard LJ, Damm D, Garrick BL, Lam A, Kapoun AM, Zheng Q, Protter AA, Schreiner GF, White RT. Altered patterns of gene expression in response to myocardial infarction. Circ Res. 2000;86:939–945.PubMedCrossRefGoogle Scholar
- 19.Friddle CJ, Koga T, Rubin EM, Bristow J. Expression profiling reveals distinct sets of genes altered during induction and regression of cardiac hypertrophy. Proc Natl Acad Sci USA. 2000;97:6745–6750.PubMedCrossRefGoogle Scholar
Copyright information
© Springer Science+Business Media New York 2001