Distinct Molecular Phenotypes in Murine Cardiac Muscle Development, Growth, and Hypertrophy

Schoenfeld, Jill; Vasser, Mark; Jhurani, Parkash; Ng, Peter A.; Hunter, John; Ross, John; Chien, Kenneth R.; Lowe, David

doi:10.1006/jmcc.1998.0787

Cited by 52 publications

(46 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All of these data are consistent with previous reports (Schoenfeld et al 1998, Wagner et al 2004. Normal adult's hearts have a high expression of α-MHC and low β-MHC level, but this is reversed in POL-induced cardiac hypertrophy (Schoenfeld et al 1998, Wagner et al 2004. The expression of α-MHC decreased and that of β-MHC increased with aortic constriction (data not shown), also consistent with previous reports.…”

Section: Cardiac Hypertrophy Correlates With Polsupporting

confidence: 93%

“…The expression of PLBN, which is important in calcium handling, decreased with aortic constriction (data not shown). All of these data are consistent with previous reports (Schoenfeld et al 1998, Wagner et al 2004. Normal adult's hearts have a high expression of α-MHC and low β-MHC level, but this is reversed in POL-induced cardiac hypertrophy (Schoenfeld et al 1998, Wagner et al 2004.…”

Section: Cardiac Hypertrophy Correlates With Polsupporting

confidence: 93%

“…The following genes were assayed using reverse transcription quantitative PCR (RT-QPCR) (Schoenfeld et al 1998, Duan et al 2005: type III collagen (Coll III), atrial natriuretic peptide (ANP), α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC), α-skeletal actin (Sk-Actin) and phospholamban (PLBN). SYBR green was used as a universal fluorescent probe and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as an endogenous control.…”

Section: Methodsmentioning

confidence: 99%

“…(This figure is in colour only in the electronic version) Cardiac gene expression correlates with cardiac hypertrophy and systolic pressure. An altered cardiac gene expression program is one of the characteristics of cardiac hypertrophy, particularly that induced by POL (Schoenfeld et al 1998, Wagner et al 2004. We used RT-QPCR to measure some of these expression levels in the ventricles with sham operation or aortic constriction using 25G, 26G, or 27G needles, and correlated them with both VW/BW and week-4 systolic pressure.…”

Section: Cardiac Hypertrophy Correlates With Polmentioning

confidence: 99%

“…Cardiac fibrosis is highly associated with POL (Brede et al 2002, McMullen et al 2003, Liao et al 2004, De Acetis et al 2005, but the correlation between fibrosis and hypertrophy or POL has not been fully investigated. Responding to POL, hearts adapt by altering the gene expression, including embryonic, contractile or cytoskeletal, calcium-handling, collective tissue and cardiac metabolism genes (Schoenfeld et al 1998, Hoshijima and Chien 2002, Wagner et al 2004. It is not fully understood to what extent POL or hypertrophy may correlate with these changes in the cardiac gene expression.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

et al. 2007

View full text Add to dashboard Cite

Pressure overload (POL) is a classical model for studying cardiac hypertrophy, but there has been no direct measure of hemodynamics in a conscious ambulatory mouse model of POL. We used abdominal aortic constriction to produce POL and radiotelemetry to measure the blood pressure and heart rate for three weeks. The cardiac size correlated with the systolic pressure in the last week is better than other hemodynamic parameters. Cardiac fibrosis was more correlated to the cardiac size than to the systolic pressure. The expression of the cardiac genes that are typically associated with cardiac hypertrophy was correlated with both cardiac size and systolic pressure. In conclusion, the systolic pressure is the major determinant of cardiac hypertrophy in the murine POL model. In contrast, cardiac fibrosis shows the influence of other factors besides systolic pressure. The combination of the POL model with continuous direct measurements of hemodynamics represents a significant technological advance and will lead to an extended usefulness of POL methodologically.

show abstract

Section: Cardiac Hypertrophy Correlates With Polsupporting

confidence: 93%

Section: Cardiac Hypertrophy Correlates With Polsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: Cardiac Hypertrophy Correlates With Polmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

et al. 2007

View full text Add to dashboard Cite

show abstract

Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy

Strøm

Kruhøffer

Knudsen

et al. 2004

Comparative and Functional Genomics

View full text Add to dashboard Cite

Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in hypertrophic signalling. From gene expression analyses (8740 probe sets, n = 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61 genes whose altered expression had previously been reported. We identified a single common gene program underlying hypertrophic remodelling, regardless of how the hypertrophy was induced. These genes constitute the molecular basis for the existence of one main form of cardiac hypertrophy and may be useful for prediction of a common therapeutic approach. Supplementary material for this article can be found at: http://www.interscience.wiley.com/jpages/1531-6912/suppmat

show abstract

Functional Genomics by cDNA Subtractive Hybridization

Depré¹

2007

Methods in Molecular Biology

View full text Add to dashboard Cite

The regulation of myocardial gene expression is highly sensitive to any extracellular or intracellular stimulus that affects contractile function. Subtractive suppression hybridization represents a large-scale, unbiased method for detecting transcriptionally and posttranscriptionally regulated genes, both known and unknown, independently of the prevalence of these transcripts. The strength of subtractive hybridization relies on its unbiased nature and its power to extract even low-abundance transcripts. Therefore, the subtraction experiments can reveal "unexpected" gene profiles and can represent a starting point for the cloning and characterization of novel genes. However, the procedure and the subsequent sequencing of the subtracted genes are labor intensive, and, because the method is purely qualitative, it also requires alternative methods of validation.

show abstract

Distinct Molecular Phenotypes in Murine Cardiac Muscle Development, Growth, and Hypertrophy

Cited by 52 publications

References 0 publications

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Direct monitoring pressure overload predicts cardiac hypertrophy in mice

Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy

Functional Genomics by cDNA Subtractive Hybridization

Contact Info

Product

Resources

About