Cardiac myocytes as targets for the action of peptide growth factors.

Schneider, Michael; Parker, Thomas G.

doi:10.1161/01.cir.81.5.1443

Cited by 108 publications

(35 citation statements)

References 105 publications

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“…The same blot was hybridized with a cDNA for GAPDH (29) Age-related Differences in Cardiac Gene Expression 943 AoC increased the mean value ofmyocyte width from 20 to 26 ,um in the adult rats but did not cause a further increase in this index in the old. On the other hand, the biochemical phenotype of the stressed myocardium of the old animals is very similar to that of the advanced hypertrophy in the young (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). This indicates that the senescent myocytes are able to sense increased load and change the pattern ofgene expression.…”

Section: Resultsmentioning

confidence: 74%

“…In addition, pressure overload has been shown to markedly increase ventricular mRNA levels of atrial natriuretic factor (ANF) (10, 16,17) and to significantly decrease the mRNA levels ofsarcoplasmic reticulum (SR) Ca2+-ATPase (18)(19)(20). Thus, hemodynamic stress changes the levels ofthese mRNA species similar to those observed during the fetal stage (10, 11,18).…”

Section: Introductionmentioning

confidence: 97%

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Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium.

Takahashi¹,

Schunkert²,

Isoyama³

et al. 1992

J. Clin. Invest.

143

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IntroductionCardiac adaptation to hemodynamic stress involves both quantitative (hypertrophy) and qualitative (pattern of gene expression) changes. Our previous studies have shown that advancing age in the rat is associated with diminished capacity to develop left ventricular hypertrophy in response to either ascending aortic constriction (AoC). In this study, we examined whether the expression of protooncogenes and contractile protein genes in response to AoC differs between adult (9-mo-old) and old (18-mo-old) rats. RNA was isolated from the left ventricles of AoC animals of both age groups subjected to a similar hemodynamic stress. Immediately after AoC, the levels of the ventricular expression ofc-fos and c-jun protooncogenes were markedly lower in the old rats than in the adult animals. 5 d after the operation, the ratio of,-to a-myosin heavy chain mRNAs increased significantly after AoC in both age groups. In contrast, AoC was associated with a marked reduction in the levels of mRNAs encoding sarcoplasmic reticulum Ca2"-ATPase (by 69%) and cardiac calsequestrin (by 49%) in the old rats but not in the adults. The mRNAs encoding atrial natriuretic factor and skeletal a-actin increased in response to AoC only in the adult rats. There were no significant differences in expression of the cardiac a-actin mRNA among the experimental groups. These data suggest that (a) the expression of protooncogenes in response to acute pressure overload is significantly reduced in the aged rats and (b) the pattern of expression of the contractile protein gene in response to AoC in the old rats differs qualitatively as well as quantitatively from that in younger animals. These age-related differences may play a role in the higher frequency of heart failure in the aged during hemodynamic stress. (J. Clin. Invest. 1992. 89:939-946.) Key words: actin . myosin heavy chain * calsequestrin * Ca2+-ATPase -atrial natriuretic factor

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Section: Resultsmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 97%

Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium.

Takahashi¹,

Schunkert²,

Isoyama³

et al. 1992

J. Clin. Invest.

143

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“…In the absence of the capability for substantive cell division, postnatal cardiac myocytes adapt to load by myocyte enlargement as well as the reinduction of a fetal pattern of cardiac gene expression. [1][2][3] It is controversial whether the external stimulus of load initiates myocyte growth via multiple intracellular signaling pathways or by a critical transcriptional pathway on which other signals converge. 4 Calcineurin is a calcium-calmodulin-dependent serine-threonine phosphatase that activates transcription factors of the NFAT family causing their translocation to the nucleus to initiate transcription of cytokines involved in the immune response.…”

mentioning

confidence: 99%

Pressure Overload Induces Severe Hypertrophy in Mice Treated With Cyclosporine, an Inhibitor of Calcineurin

Ding

Price

Borg

et al. 1999

Circulation Research

134

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Abstract-Cardiac hypertrophy is the fundamental adaptation of the adult heart to mechanical load. Recent work has shown that inhibition of calcineurin activity with cyclosporine suppresses the development of hypertrophy in calcineurin transgenic mice and in in vitro systems of neonatal rat cardiocytes stimulated with peptide growth factors. To test the hypothesis that the calcineurin signaling pathway is critical for load-induced hypertrophy in vivo, we examined the effects of cyclosporine treatment on left ventricular hypertrophy induced by experimental ascending aortic stenosis for 4 weeks in mice. Left ventricular systolic pressure was elevated to a similar level in aortic stenosis mice that were treated with cyclosporine versus no drug. Left ventricular mass and myocyte size were similar in treated and untreated aortic stenosis animals and significantly greater than control animals, showing that cyclosporine treatment does not suppress hypertrophic growth. Both treated and untreated animals showed increased left ventricular expression of the load-sensitive gene atrial natriuretic factor. Calcineurin activity was measured in the left ventricle and the spleen from control mice and aortic stenosis mice treated with cyclosporine versus no drug. Levels of calcineurin activity were similar in the spleens of control and untreated aortic stenosis mice. However, calcineurin activity was severely depressed in left ventricular tissue of untreated aortic stenosis mice compared with control mice and was further reduced by cyclosporine treatment. Thus, pathological hypertrophy and cardiac-restricted gene expression induced by pressure overload in vivo are not suppressed by treatment with cyclosporine and do not appear to depend on the elevation of left ventricular calcineurin activity. (Circ Res. 1999;84:729-734.)

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“…The myocardium is composed of many different cell types with cardiac myocytes contributing the greatest protein mass. In response to hormonal (polypeptide growth factors, endothelin, angiotensin II) and mechanical stimuli (1)(2)(3)(4)(5)(6), the myocardium adapts by hypertrophy of individual myocytes. Because these cells are terminally differentiated cells that have lost the ability to proliferate, cardiac growth during hypertrophy results primarily from an increase in cellular protein content, with little or no change in cardiac myocyte number (7).…”

mentioning

confidence: 99%

Insulin-like Growth Factor-I Rapidly Activates Multiple Signal Transduction Pathways in Cultured Rat Cardiac Myocytes

Foncea¹,

Andersson²,

Ketterman³

et al. 1997

Journal of Biological Chemistry

186

103

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Cardiac myocytes as targets for the action of peptide growth factors.

Cited by 108 publications

References 105 publications

Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium.

Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium.

Pressure Overload Induces Severe Hypertrophy in Mice Treated With Cyclosporine, an Inhibitor of Calcineurin

Insulin-like Growth Factor-I Rapidly Activates Multiple Signal Transduction Pathways in Cultured Rat Cardiac Myocytes

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