Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Izumo, Seigo; Lompré, Anne‐Marie; Matsuoka, Rumiko; Koren, G.; Schwartz, Ketty; Nadal-Ginard, B; Mahdavi, Vijak

doi:10.1172/jci112908

Cited by 431 publications

(219 citation statements)

References 49 publications

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“…To validate the model, we examined the expression of two genes, ␣-myosin heavy chain (␣-MHC) and ␣-skeletal actin. ␣-MHC promoter activity does not change after CoA (20), and published results suggest that mRNA levels do not change significantly (21) or decrease by 54% (20) by 7 days post-CoA. In our CoA group, the ␣-MHC promoter-containing plasmid, pSV0MCAT, was expressed at approximately 90% of the level of the control group, which was not significantly different (Fig.…”

Section: Resultssupporting

confidence: 47%

Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Herzig

Jobe

Aoki

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

183

125

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Hypertrophy of mammalian cardiac muscle is mediated, in part, by angiotensin II through an angiotensin II type 1a receptor (AT 1a R)-dependent mechanism. To understand how the level of AT 1a Rs is altered in this pathological state, we studied the expression of an injected AT 1a R promoter-luciferase reporter gene in adult rat hearts subjected to an acute pressure overload by aortic coarctation. This model was validated by demonstrating that coarctation increased expression of the ␣-skeletal actin promoter 1.7-fold whereas the ␣-myosin heavy chain promoter was unaffected. Pressure overload increased expression from the AT 1a R promoter by 1.6-fold compared with controls. Mutations introduced into consensus binding sites for AP-1 or GATA transcription factors abolished the pressure overload response but had no effect on AT 1a R promoter activity in control animals. In extracts from coarcted hearts, but not from control hearts, a Fos-JunB-JunD complex and GATA-4 were detected in association with the AP-1 and GATA sites, respectively. These results establish that the AT 1a R promoter is active in cardiac muscle and its expression is induced by pressure overload, and suggest that this response is mediated, in part, by a functional interaction between AP-1 and GATA-4 transcription factors.Pathological conditions resulting in increased cardiac workload generally are associated with activation of systemic and local renin-angiotensin systems and increased levels of circulating angiotensin II (AngII) (1, 2). However, little is understood about how AngII type 1a receptors (AT 1a R) are modulated under these same pathological conditions. AngII is a potent growth factor that mediates the hypertrophic growth of cardiac muscle cells and is a chemical mediator of stretchinduced cardiomyocyte hypertrophy (3-7). The interaction of AngII with AT 1a R activates a signal transduction cascade that effects the phosphorylation of serum response factor and p62 TCF by pp90 RSK and mitogen-activated protein kinase, respectively, resulting in increased c-fos gene expression (5-7). Hypertrophic stimuli also increase the level of AT1 a R mRNA in cardiomyocytes. A 3-fold increase in AT 1a R mRNA and a 2-fold increase in AT 1a R densities have been reported in spontaneously hypertensive and two kidney one-clip renovascular hypertensive rats with established cardiac hypertrophy (8). It is not known whether this increase in AT 1a R mRNA is mediated by a transcriptional or posttranscriptional mechanism.In this study, we use direct injection of DNA into the heart in conjunction with aortic coarctation (CoA) to study the activity of the AT 1a R promoter in the normal and pressureoverloaded rat heart. The AT 1a R promoter was found to be active in normal adult cardiac muscle, whereas gene expression was increased in response to an acute pressure overload (PO). The induced expression was blocked by mutation of either an AP-1 or a GATA binding site, however, these mutations had no effect on basal expression. Administration of the angiotensin-...

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Section: Resultssupporting

confidence: 47%

Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Herzig

Jobe

Aoki

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

183

125

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“…Among these, possible candidates for PC's effect included genes related to cell signaling (Nkiras2), cell adhesion (Itgb1, Nrp1), stress responses (Hmox1), and muscle contractile function (Myh7, Tpm1). Importantly, myosin heavy-chain (MHC) isoform switch (increased ␤-MHC with decreased ␣-MHC expression), an established fetal-type gene reexpression characteristic of load-dependent hypertrophy (14), was reversed after PC treatment.…”

Section: Effect Of Pc On Gene Expression Profilesmentioning

confidence: 99%

Activated vitamin D attenuates left ventricular abnormalities induced by dietary sodium in Dahl salt-sensitive animals

Bodyak

Ayus²,

Achinger³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

304

250

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Observations in hemodialysis patients suggest a survival advantage associated with activated vitamin D therapy. Left ventricular (LV) structural and functional abnormalities are strongly linked with hemodialysis mortality. Here, we investigated whether paricalcitol (PC, 19-nor-1,25(OH)2D2), an activated vitamin D compound, attenuates the development of LV abnormalities in the Dahl salt-sensitive (DSS) rat and whether humans demonstrate comparable findings. Compared with DSS rats fed a high-salt (HS) diet (6% NaCl for 6 weeks), HS؉PC was associated with lower heart and lung weights, reduced LV mass, posterior wall thickness and end diastolic pressures, and increased fractional shortening. Blood pressures did not significantly differ between the HS groups. Plasma brain natriuretic peptide levels, and cardiac mRNA expression of brain natriuretic peptide, atrial natriuretic factor, and renin were significantly reduced in the HS؉PC animals. Microarray analyses revealed 45 specific HS genes modified by PC. In a retrospective pilot study of hemodialysis patients, PC-treated subjects demonstrated improved diastolic function and a reduction in LV septal and posterior wall thickness by echocardiography compared with untreated patients. In summary, PC attenuates the development of LV alterations in DSS rats, and these effects should be examined in human clinical trials.cardiac hypertrophy ͉ heart failure ͉ paricalcitol ͉ renal failure T he rate of cardiovascular-related mortality in hemodialysis patients is 10-20 times higher than that observed in the general population (1). Left ventricular hypertrophy (LVH) and diastolic dysfunction are present in Ͼ50% of patients at dialysis initiation, and these abnormalities are strongly linked with dialysis-related mortality (2). Currently, there are no well accepted means to modify cardiac structural and functional alterations in renal-failure patients.We recently demonstrated in observational studies that therapy with activated vitamin D to chronic hemodialysis patients is associated with reduction in cardiovascular-related mortality (3, 4). Conversion of nutritional vitamin D (25(OH)D 3 ) to the hormonally active form of vitamin D (1,25(OH) 2 D 3 ) occurs primarily in the kidney; thus, patients with kidney failure commonly present with altered vitamin D status (5). There is growing evidence that vitamin D either directly or indirectly affects cardiac structure and function. The vitamin D receptor knockout mouse model demonstrates increased cardiac renin expression and marked cardiomyocyte hypertrophy (6), and 1,25(OH) 2 D 3 attenuates cardiomyocyte proliferation (7) and hypertrophy (8) in vitro. Here, we demonstrate that treatment with an activated vitamin D compound attenuates the development of cardiac hypertrophy and dysfunction in a recognized animal model of such abnormalities and that comparable findings are evident in humans.

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“…It has been demonstrated that chronic pressure overload to the heart alters the expression of genes for contractile elements, growth factors, and proto-oncogenes in the heart [2][3][4].…”

Section: Animals and Surgical Proceduresmentioning

confidence: 99%

Increased production of endothelin‐1 in the hypertrophied rat heart due to pressure overload

et al. 1993

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Endothelin-1 (ET-l) has been demonstrated to induce hypertrophy in cultured cardiac myocytes. We investigated the production of ET-l in the heart of aorta-banded rats in vivo. Seven days after the banding of the abdominal aorta, rats developed a significant left ventricular hypertrophy. The tissue content of mature ET-1 and the level of expression of prepro ET-l mRNA were higher in the left ventricle of aorta-banded rats than in those of sham-operated rats. The expression of prepro ET-l mRNA in the right ventricle was not different between the two groups. These tindings indicate that the production of ET-l increased in the hypertrophied left ventricle, thereby suggesting the possible involvement of endogenous ET-l in the development of cardiac hypertrophy due to pressure overload.

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Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Cited by 431 publications

References 49 publications

Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Activated vitamin D attenuates left ventricular abnormalities induced by dietary sodium in Dahl salt-sensitive animals

Increased production of endothelin‐1 in the hypertrophied rat heart due to pressure overload

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Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.

Cited by 431 publications

References 49 publications

Angiotensin II type 1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Angiotensin II type 1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Activated vitamin D attenuates left ventricular abnormalities induced by dietary sodium in Dahl salt-sensitive animals

Increased production of endothelin‐1 in the hypertrophied rat heart due to pressure overload

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Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload

Angiotensin II type _1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload