Stimulatory effect of dexamethasone on angiotensin-converting enzyme in neonatal rat cardiac myocytes

Barreto‐Chaves, Maria Luíza Morais; Heimann, Andrea S.

doi:10.1590/s0100-879x2000000600007

Cited by 36 publications

(22 citation statements)

References 10 publications

(10 reference statements)

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“…Primary cultures of neonatal rat cardiomyocytes were prepared by enzymatic disaggregation, as described previously by us [3]. Hearts from neonatal (1-3 days old) Wistar rats were excised and ventricles were subjected to multiple enzymatic digestions at 37°C, using a mixture of collagenase type 2 (Worthington, Lakewood, New Jersey, USA) and pancreatin (Life Technologies, Carlsbad, California, USA).…”

Section: Primary Cultures Of Cardiomyocytesmentioning

confidence: 99%

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

et al. 2015

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Elevated thyroid hormone (TH) levels induce cardiac hypertrophy partially via type 1 Angiotensin II receptor (AT1R). MicroRNAs (miRNAs) are key regulators of cardiac homeostasis, and miR-133 has been shown to be involved in cardiac hypertrophy. However, the potential role of miR-133 in cardiac growth induced by TH is unknown. Thus, we aimed to investigate the miR-133 expression, as well as its potential role in cardiac hypertrophy in response to TH. Wistar rats were subjected to hyperthyroidism combined or not with the AT1R blocker. T3 serum levels were assessed to confirm the hyperthyroid status. TH induced cardiac hypertrophy, as evidenced by higher cardiac weight/tibia length ratio and α-actin mRNA levels, which was prevented by AT1R blocker. miR-133 expression was decreased in TH-induced cardiac hypertrophy in part through the AT1R. Additionally, the cardiac mRNA levels of miR-133 targets, SERCA2a and calcineurin were increased in hyperthyroidism partially via AT1R, as evaluated by real-time RT-PCR. Interestingly, miR-133 levels were unchanged in T3-induced cardiomyocyte hypertrophy in vitro. However, a gain-of-function study revealed that miR-133 mimic blunted the T3-induced cardiomyocyte hypertrophy in vitro. Together, our data indicate that miR-133 expression is reduced in TH-induced cardiac hypertrophy partially by the AT1R and that miR-133 mimic prevents the cardiomyocyte hypertrophy in response to T3 in vitro. These findings provide new insights regarding the mechanisms involved in the cardiac growth mediated by TH, suggesting that miR-133 plays a key role in TH-induced cardiomyocyte hypertrophy.

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Section: Primary Cultures Of Cardiomyocytesmentioning

confidence: 99%

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

et al. 2015

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“…Primary cultures of neonatal rat ventricular cardiac myocytes were prepared by enzymatic disaggregation, as described previously (Barreto-Chaves et al 2000). Briefly, hearts from neonatal (1-to 3-day old) Wistar rats were excised and ventricles were minced and subjected to multiple enzymatic digestions at 37 8C using a mixture of collagenase type 2 (Worthington, Lakewood, NJ, USA) and pancreatin (Gibco).…”

Section: Primary Cultures Of Cardiomyocytesmentioning

confidence: 99%

New insight into the mechanisms associated with the rapid effect of T3 on AT1R expression

Diniz

Takano²,

Bruneto³

et al. 2012

Journal of Molecular Endocrinology

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The angiotensin II type 1 receptor (AT1R) is involved in the development of cardiac hypertrophy promoted by thyroid hormone. Recently, we demonstrated that triiodothyronine (T 3 ) rapidly increases AT1R mRNA and protein levels in cardiomyocyte cultures. However, the molecular mechanisms responsible for these rapid events are not yet known. In this study, we investigated the T 3 effect on AT1R mRNA polyadenylation in cultured cardiomyocytes as well as on the expression of microRNA-350 (miR-350), which targets AT1R mRNA. The transcriptional and translational actions mediated by T 3 on AT1R levels were also assessed. The total content of ubiquitinated proteins in cardiomyocytes treated with T 3 was investigated. Our data confirmed that T 3 rapidly raised AT1R mRNA and protein levels, as assessed by realtime PCR and western blotting respectively. The use of inhibitors of mRNA and protein synthesis prevented the rapid increase in AT1R protein levels mediated by T 3 . In addition, T 3 rapidly increased the poly-A tail length of the AT1R mRNA, as determined by rapid amplification of cDNA ends poly-A test, and decreased the content of ubiquitinated proteins in cardiomyocytes. On the other hand, T 3 treatment increased miR-350 expression. In parallel with its transcriptional and translational effects on the AT1R, T 3 exerted a rapid posttranscriptional action on AT1R mRNA polyadenylation, which might be contributing to increase transcript stability, as well as on translational efficiency, resulting to the rapid increase in AT1R mRNA expression and protein levels. Finally, these results show, for the first time, that T 3 rapidly triggers distinct mechanisms, which might contribute to the regulation of AT1R levels in cardiomyocytes.

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“…The renin-angiotensin system (RAS) is important for development and growth of the neonatal heart and neonatal piglets treated with angiotensin converting enzyme (ACE) inhibitors develop a decreased cardiac growth rate [80]. In rat cardiomyocytes, dexamethasone up-regulates expression of Aogen and ACE resulting in a marked hypertrophy of the left ventricle [81]. Still, it is not known if this effect depends solely on the cardiac RAS or if the circulatory / renal RAS is involved.…”

Section: Hormones: Thyoxine and Steroidsmentioning

confidence: 99%

New Inotropic Pharmacologic Strategies Targeting the Failing Myocardiumin the Newborn and Infant

Veldman

Rupp²,

Schranz³

2006

MRMC

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Pharmacologic support of the failing neonatal heart to maintain cardiac output, which is vital for sufficient end organ perfusion, is a challenging task for the pediatric intensivist, especially since strategies which have been proven to be effective in adults cannot necessarily be extrapolated to neonates. The unique biochemical properties and structure of the neonatal heart, including the increased non-contractile tissue mass, a lower responsiveness to beta adrenergic agents and the heart rate dependent cardiac output with a limited ability to increase stroke volume, favor some of the new inotropes of the Ca+ sensitizer family. Focusing on the after load reduction, inodilators as phosphodiesterase inhibitors and human brain natriuretic peptide offer treatment options for the neonatal myocardium. Additionally, thyroxine and steroids have been investigated in neonates with low cardiac output after surgery for congenital heart disease. Gene therapy, in particular cardiac-selective gene transfer, might offer perspectives for future support for the neonatal heart. This text reviews some of the most recent pharmacologic strategies targeting the failing myocardium in the critically ill newborn and infant.

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Stimulatory effect of dexamethasone on angiotensin-converting enzyme in neonatal rat cardiac myocytes

Cited by 36 publications

References 10 publications

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

New insight into the mechanisms associated with the rapid effect of T3 on AT1R expression

New Inotropic Pharmacologic Strategies Targeting the Failing Myocardiumin the Newborn and Infant

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