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Article: Microarray gene expression profiles in dilated and hypertrophic cardiomyopathic end-stage heart failure.

TitleMicroarray gene expression profiles in dilated and hypertrophic cardiomyopathic end-stage heart failure.
Authors
KeywordsCdna Microarray
Normalization
Real-Time Reverse Transcription-Polymerase Chain Reaction
Issue Date2002
Citation
Physiol Genomics, 2002, v. 10 n. 1, p. 31-44 How to Cite?
AbstractDespite similar clinical endpoints, heart failure resulting from dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) appears to develop through different remodeling and molecular pathways. Current understanding of heart failure has been facilitated by microarray technology. We constructed an in-house spotted cDNA microarray using 10,272 unique clones from various cardiovascular cDNA libraries sequenced and annotated in our laboratory. RNA samples were obtained from left ventricular tissues of precardiac transplantation DCM and HCM patients and were hybridized against normal adult heart reference RNA. After filtering, differentially expressed genes were determined using novel analyzing software. We demonstrated that normalization for cDNA microarray data is slide-dependent and nonlinear. The feasibility of this model was validated by quantitative real-time reverse transcription-PCR, and the accuracy rate depended on the fold change and statistical significance level. Our results showed that 192 genes were highly expressed in both DCM and HCM (e.g., atrial natriuretic peptide, CD59, decorin, elongation factor 2, and heat shock protein 90), and 51 genes were downregulated in both conditions (e.g., elastin, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). We also identified several genes differentially expressed between DCM and HCM (e.g., alphaB-crystallin, antagonizer of myc transcriptional activity, beta-dystrobrevin, calsequestrin, lipocortin, and lumican). Microarray technology provides us with a genomic approach to explore the genetic markers and molecular mechanisms leading to heart failure.
Persistent Identifierhttp://hdl.handle.net/10722/148306
ISSN
2015 Impact Factor: 2.615
2015 SCImago Journal Rankings: 1.545
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHwang, JJen_US
dc.contributor.authorAllen, PDen_US
dc.contributor.authorTseng, GCen_US
dc.contributor.authorLam, CWen_US
dc.contributor.authorFananapazir, Len_US
dc.contributor.authorDzau, VJen_US
dc.contributor.authorLiew, CCen_US
dc.date.accessioned2012-05-29T06:12:07Z-
dc.date.available2012-05-29T06:12:07Z-
dc.date.issued2002en_US
dc.identifier.citationPhysiol Genomics, 2002, v. 10 n. 1, p. 31-44en_US
dc.identifier.issn1094-8341en_US
dc.identifier.urihttp://hdl.handle.net/10722/148306-
dc.description.abstractDespite similar clinical endpoints, heart failure resulting from dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) appears to develop through different remodeling and molecular pathways. Current understanding of heart failure has been facilitated by microarray technology. We constructed an in-house spotted cDNA microarray using 10,272 unique clones from various cardiovascular cDNA libraries sequenced and annotated in our laboratory. RNA samples were obtained from left ventricular tissues of precardiac transplantation DCM and HCM patients and were hybridized against normal adult heart reference RNA. After filtering, differentially expressed genes were determined using novel analyzing software. We demonstrated that normalization for cDNA microarray data is slide-dependent and nonlinear. The feasibility of this model was validated by quantitative real-time reverse transcription-PCR, and the accuracy rate depended on the fold change and statistical significance level. Our results showed that 192 genes were highly expressed in both DCM and HCM (e.g., atrial natriuretic peptide, CD59, decorin, elongation factor 2, and heat shock protein 90), and 51 genes were downregulated in both conditions (e.g., elastin, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). We also identified several genes differentially expressed between DCM and HCM (e.g., alphaB-crystallin, antagonizer of myc transcriptional activity, beta-dystrobrevin, calsequestrin, lipocortin, and lumican). Microarray technology provides us with a genomic approach to explore the genetic markers and molecular mechanisms leading to heart failure.en_US
dc.languageengen_US
dc.relation.ispartofPhysiol Genomicsen_US
dc.subjectCdna Microarray-
dc.subjectNormalization-
dc.subjectReal-Time Reverse Transcription-Polymerase Chain Reaction-
dc.subject.meshAdulten_US
dc.subject.meshAorta - Chemistry - Metabolismen_US
dc.subject.meshAortic Diseases - Geneticsen_US
dc.subject.meshCardiomyopathy, Dilated - Geneticsen_US
dc.subject.meshCardiomyopathy, Hypertrophic - Geneticsen_US
dc.subject.meshDna, Complementary - Geneticsen_US
dc.subject.meshFetal Heart - Chemistry - Metabolismen_US
dc.subject.meshGene Expression Profiling - Methods - Statistics & Numerical Dataen_US
dc.subject.meshGene Expression Regulation - Geneticsen_US
dc.subject.meshGene Libraryen_US
dc.subject.meshGenes - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshMyocardium - Chemistry - Metabolismen_US
dc.subject.meshOligonucleotide Array Sequence Analysis - Methods - Statistics & Numerical Dataen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleMicroarray gene expression profiles in dilated and hypertrophic cardiomyopathic end-stage heart failure.en_US
dc.typeArticleen_US
dc.identifier.emailLam, CW:ching-wanlam@pathology.hku.hken_US
dc.identifier.authorityLam, CW=rp00260en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid12118103en_US
dc.identifier.scopuseid_2-s2.0-0345806493en_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage31en_US
dc.identifier.epage44en_US
dc.identifier.isiWOS:000176749000005-
dc.publisher.placeUnited Statesen_US

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