Identification of Differentially Expressed Genes in Cardiac Hypertrophy by Analysis of Expressed Sequence Tags

Hwang, David; Dempsey, Adam A.; Lee, Cheuk-Yu; Liew, Choong‐Chin

doi:10.1006/geno.2000.6171

Cited by 101 publications

(69 citation statements)

References 72 publications

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“…Therefore, 16,616 (38.5%) of the SUCEST clusters could potentially represent new genes. These values are comparable to those found for ESTs sequences from other organisms (Hwang et al 2000;Adams et al 1992;Claverie 1996). Ascribing functions to those anonymous sequences has therefore become one of the major bottlenecks in plant and animal genomics.…”

Section: Quality Controlsupporting

confidence: 86%

The libraries that made SUCEST

et al. 2001

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A large-scale sequencing of sugarcane expressed sequence tags (ESTs) was carried out as a first step in depicting the genome of this important tropical crop. Twenty-six unidirectional cDNA libraries were constructed from a variety of tissues sampled from thirteen different sugarcane cultivars. A total of 291,689 cDNA clones were sequenced in their 5' and 3'end regions. After trimming low-quality sequences and removing vector and ribosomal RNA sequences, 237,954 ESTs potentially derived from protein-encoding messenger RNA (mRNA) remained. The average insert size in all libraries was estimated to be 1,250bp with the insert length varying from 500 to 5,000 bp. Clustering the 237,954 sugarcane ESTs resulted in 43,141clusters, from which 38% had no matches with existing sequences in the public databases. Around 53% of the clusters were formed by ESTs expressed in at least two libraries while 47% of the clusters are formed by ESTs expressed in only one library. A global analysis of the ESTs indicated that around 33% contain cDNA clones with full-length insert.

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Section: Quality Controlsupporting

confidence: 86%

The libraries that made SUCEST

et al. 2001

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“…60 Thus decorin up-regulation could be a counteraction to tissue necrosis, interfering with tissue remodeling by fibrosis. 26,27 Elevation in the expression of decorin was recently reported in two cases in myocardial infarction 61,62 and one in cardiac hypertrophy, 63 all of which displayed fibrosis. The two more recent cases were also elaborated by global gene expression analysis.…”

Section: Discussionmentioning

confidence: 91%

“…The two more recent cases were also elaborated by global gene expression analysis. 62,63 Decorin has the ability to bind and neutralize TGF-␤1 and potentially abrogate its effect on tissue fibrosis. 26,27 On the other hand TGF-␤1 has the potential to initiate the production of decorin.…”

Section: Discussionmentioning

confidence: 99%

Extensive Induction of Important Mediators of Fibrosis and Dystrophic Calcification in Desmin-Deficient Cardiomyopathy

Mavroidis

Capetanaki

2002

The American Journal of Pathology

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Mice lacking the intermediate filament protein desmin demonstrate abnormal mitochondria behavior, disruption of muscle architecture, and myocardial degeneration with extensive calcium deposits and fibrosis. These abnormalities are associated with cardiomyocyte hypertrophy, cardiac chamber dilation and eventually with heart failure. In an effort to elucidate the molecular mechanisms leading to the observed pathogenesis, we have analyzed gene expression changes in cardiac tissue using differential display polymerase chain reaction and cDNA atlas array methods. The most substantial changes were found in genes coding the small extracellular matrix proteins osteopontin and decorin that are dramatically induced in the desmin-null myocardium. We further analyzed their expression pattern both at the RNA and protein levels and we compared their spatial expression with the onset of calcification. Extensive osteopontin localization is observed by immunohistochemistry in the desmin-null myocardium in areas with massive myocyte death, as well as in hypercellular regions with variable degrees of calcification and fibrosis. Osteopontin is consistently co-localized with calcified deposits, which progressively are transformed to psammoma bodies surrounded by decorin, especially in the right ventricle. These data together with the observed up-regulation of transforming growth factor-␤1 and angiotensin-converting enzyme, could explain the extensive fibrosis and dystrophic calcification observed in the heart of desminnull mice, potentially crucial events leading to heart failure. Ablation of desmin, the muscle-specific intermediate filament protein, by gene targeting in mice leads to transient cardiomyocyte hypertrophy and extensive cardiomyocyte death, followed by cardiac chamber dilation and heart failure.

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“…Overexpression of MMP-9, a gelatinase B whose substrates include gelatin, collagen IV, V, and XIV, aggrecan, elastin, entactin, and vibronectin, 34 as previously reported in LVH in humans. 35 These genes could be involved in the pathophysiological mechanisms leading to the genesis and progression of heart failure. We also found upregulation, in both chambers, of mRNA levels encoding proteins of the mitochondria respiratory chain such as cytochrome C oxidase subunit I and VIIb, NADH dehydrogenase, and ATP synthase F0 subunit.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Transcriptome Analysis in Obesity-Related Hypertension

et al. 2003

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Abstract-Obesity is associated with volumetric arterial hypertension and with early increase in heart rate and decreased heart rate variability. The consequences of obesity-related hypertension on heart gene regulation are poorly known and were investigated in a model of obesity-related hypertension induced by high fat diet in dogs. When compared with control animals (nϭ6), a 9-week high fat diet (nϭ6) provoked significant weight gain and increased blood pressure load and heart rate but failed to significantly change left ventricular mass assessed by echocardiography. Subtractive hybridization of dog heart cDNA libraries were used to generate sublibraries containing differentially expressed cDNAs that were in turn spotted onto membranes to create custom microarrays. Hybridizations of these microarrays with complex probes representing mRNAs expressed in right atria and left ventricles from obese hypertensive and control dogs were performed. Thirty-eight differentially expressed genes were identified; altered expression was confirmed by Northern blot analysis in 15. In addition, real-time quantitative polymerase chain reaction confirmed differential expression for 80% of the randomly chosen tested genes. Once identified, transcripts were categorized into groups involved in metabolism, cell signaling, ionic regulation, cell proliferation, protein synthesis, and tissue remodeling. In addition, we found a set of 11 cDNAs encoding proteins with unknown functions. This study clearly shows that obesity-related hypertension, lasting for only 9 weeks, causes marked changes in gene expression in right atrium as well as the left ventricle that may contribute to early functional changes in heart function and to long-term structural changes such as left ventricular hypertrophy and remodeling. Key Words: obesity Ⅲ hypertension, arterial Ⅲ heart rate Ⅲ heart Ⅲ dogs O besity is the most prevalent nutritional disorder in developed countries 1 and plays an important role in cardiovascular morbidity through multiple mechanisms, 2 including well-known risk factors such as hypertension, 3 diabetes, 4,5 and dyslipidemia. 6 -8 Moreover, as suggested for leptine and arterial hypertension, 9 a direct interaction of adipose tissue, through its multiple secretions, with the cardiovascular system could also be involved in the pathophysiology of cardiovascular disorders associated with obesity. Previous studies have shown that overweight is associated with increased cardiac output 10 and resting heart rate and with decreased heart rate variability, 11 which is considered to be a prognostic indicator of cardiovascular mortality in humans. 12,13 Obesity is also associated with structural changes in the heart, including eccentric and concentric hypertrophy, 14 thus explaining the increased risk of cardiac failure. 15 However, the molecular mechanisms underlying these changes in cardiac function and structure are poorly understood. We and others have developed a dietary model of obesity-related hypertension that closely mimics the cardiovascular...

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Identification of Differentially Expressed Genes in Cardiac Hypertrophy by Analysis of Expressed Sequence Tags

Cited by 101 publications

References 72 publications

The libraries that made SUCEST

The libraries that made SUCEST

Extensive Induction of Important Mediators of Fibrosis and Dystrophic Calcification in Desmin-Deficient Cardiomyopathy

Cardiac Transcriptome Analysis in Obesity-Related Hypertension

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