TY - JOUR
T1 - Gene expression profiles in end-stage human idiopathic dilated cardiomyopathy
T2 - Altered expression of apoptotic and cytoskeletal genes
AU - Yung, Christina K.
AU - Halperin, Victoria L.
AU - Tomaselli, Gordon F.
AU - Winslow, Raimond L.
N1 - Funding Information:
The authors thank Dr. Joe Garcia and Dr. Shui Ye of the Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, for use of their facility and their guidance in performing the hybridization experiments. This research was supported by NIH/NHLBI U01HL66583, the Falk Medical Trust, the Whitaker Foundation, and IBM Corp. C.K. Yung is partially supported by the Natural Sciences and Engineering Research Council of Canada.
PY - 2004/2
Y1 - 2004/2
N2 - Dilated cardiomyopathy is now the leading cause of cardiovascular morbidity and mortality. While the molecular basis of this disease remains uncertain, evidence is emerging that gene expression profiles of left ventricular myocardium isolated from failing versus nonfailing patients differ dramatically. In this study, we use high-density oligonucleotide microarrays with ~22,000 probes to characterize differences in the expression profiles further. To facilitate interpretation of experimental data, we evaluate algorithms for normalization of hybridization data and for computation of gene expression indices using a control spike-in data set. We then use these methods to identify statistically significant changes in the expression levels of genes not previously implicated in the molecular phenotype of heart failure. These regulated genes take part in diverse cellular processes, including transcription, apoptosis, sarcomeric and cytoskeletal function, remodeling of the extracellular matrix, membrane transport, and metabolism.
AB - Dilated cardiomyopathy is now the leading cause of cardiovascular morbidity and mortality. While the molecular basis of this disease remains uncertain, evidence is emerging that gene expression profiles of left ventricular myocardium isolated from failing versus nonfailing patients differ dramatically. In this study, we use high-density oligonucleotide microarrays with ~22,000 probes to characterize differences in the expression profiles further. To facilitate interpretation of experimental data, we evaluate algorithms for normalization of hybridization data and for computation of gene expression indices using a control spike-in data set. We then use these methods to identify statistically significant changes in the expression levels of genes not previously implicated in the molecular phenotype of heart failure. These regulated genes take part in diverse cellular processes, including transcription, apoptosis, sarcomeric and cytoskeletal function, remodeling of the extracellular matrix, membrane transport, and metabolism.
KW - Cardiovascular genomics
KW - Dilated cardiomyopathy
KW - Gene expression
KW - Heart failure
KW - Oligonucleotide microarray
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U2 - 10.1016/j.ygeno.2003.08.007
DO - 10.1016/j.ygeno.2003.08.007
M3 - Article
C2 - 14706457
AN - SCOPUS:0346098139
SN - 0888-7543
VL - 83
SP - 281
EP - 297
JO - Genomics
JF - Genomics
IS - 2
ER -