scholarly journals Lymphoangiocrine signals promote cardiac growth and repair

Nature ◽  
2020 ◽  
Vol 588 (7839) ◽  
pp. 705-711 ◽  
Author(s):  
Xiaolei Liu ◽  
Ester De la Cruz ◽  
Xiaowu Gu ◽  
Laszlo Balint ◽  
Michael Oxendine-Burns ◽  
...  
Keyword(s):  
Cardiac Growth

scholarly journals The A-to-I RNA Editing Enzyme Adar1 Is Essential for Normal Embryonic Cardiac Growth and Development

2020 ◽  
Vol 127 (4) ◽  
pp. 550-552
Author(s):  
Joseph B. Moore ◽  
Ghazal Sadri ◽  
Annalara G. Fischer ◽  
Tyler Weirick ◽  
Giuseppe Militello ◽  
...  
Keyword(s):  
Rna Editing ◽  
Growth And Development ◽  
Cardiac Growth ◽  
Editing Enzyme

51 C/EBPβ CONTROLS EXERCISE-INDUCED CARDIAC GROWTH AND PROTECTS AGAINST PATHOLOGICAL CARDIAC REMODELING

2011 ◽  
Vol 12 (1) ◽  
pp. 11
Author(s):  
P. Bostrom ◽  
N. Mann ◽  
J. Wu ◽  
P.A. Quintero ◽  
E.R. Plovie ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Cardiac Growth ◽  
Exercise Induced

scholarly journals Overexpression of antizyme in the hearts of transgenic mice prevents the isoprenaline-induced increase in cardiac ornithine decarboxylase activity and polyamines, but does not prevent cardiac hypertrophy

2000 ◽  
Vol 350 (3) ◽  
pp. 645-653 ◽  
Author(s):  
Caroline A. MACKINTOSH ◽  
David J. FEITH ◽  
Lisa M. SHANTZ ◽  
Anthony E. PEGG
Keyword(s):  
Transgenic Mice ◽  
Ornithine Decarboxylase ◽  
Prolonged Exposure ◽  
Constitutive Expression ◽  
Decarboxylase Activity ◽  
Cardiac Growth ◽  
Polyamine Content ◽  
Transgenic Lines ◽  
Response To Stress ◽  
Polyamine Uptake

Two lines of transgenic mice were produced with constitutive expression of antizyme-1 in the heart, driven from the cardiac α-myosin heavy chain promoter. The use of engineered antizyme cDNA in which nucleotide 205 had been deleted eliminated the need for polyamine-mediated frameshifting, normally necessary for translation of antizyme mRNA, and thus ensured the constitutive expression of antizyme. Antizyme-1 is thought to be a major factor in regulating cellular polyamine content, acting both to inhibit ornithine decarboxylase (ODC) activity and to target it for degradation, as well as preventing polyamine uptake. The two transgenic lines had substantial, but different, levels of antizyme in the heart, as detected by Western blotting and by the ability of heart extracts to inhibit exogenous purified ODC. Despite the high levels of antizyme, endogenous ODC activity was not completely abolished, with 10– 39% remaining, depending on the transgenic line. Additionally, a relatively small decrease (30–32%) in cardiac spermidine content was observed, with levels of putrescine and spermine unaffected. Interestingly, although the two lines of transgenic mice had different antizyme expression levels, they had almost identical cardiac polyamine content. When treated with a single acute dose of isoprenaline (isoproterenol), cardiac ODC activity and putrescine content were substantially increased (by 14-fold and 4.7-fold respectively) in non-transgenic littermate mice, but these increases were completely prevented in the transgenic mice from both founder lines. Prolonged exposure to isoprenaline also caused increases in cardiac ODC activity and polyamine content, as well as an increase in cardiac growth, in non-transgenic mice. Although the increases in cardiac ODC activity and polyamine content were prevented in the transgenic mice from both founder lines, the increase in cardiac growth was unaffected. These transgenic mice thus provide a valuable model system in which to study the importance of polyamine levels in cardiac growth and electrophysiology in response to stress.

scholarly journals Branched chain amino acids selectively promote cardiac growth at the end of the awake period

2021 ◽  
Vol 157 ◽  
pp. 31-44
Author(s):  
Mary N. Latimer ◽  
Ravi Sonkar ◽  
Sobuj Mia ◽  
Isabelle Robillard Frayne ◽  
Karen J. Carter ◽  
...  
Keyword(s):  
Amino Acids ◽  
Branched Chain Amino Acids ◽  
Cardiac Growth ◽  
Branched Chain

scholarly journals Microtubules orchestrate local translation to enable cardiac growth

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Emily A. Scarborough ◽  
Keita Uchida ◽  
Maria Vogel ◽  
Noa Erlitzki ◽  
Meghana Iyer ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Cell Periphery ◽  
Local Translation ◽  
Microtubule Network ◽  
Critical Determinant ◽  
Translation Rate ◽  
Cardiac Growth ◽  
Translational Machinery ◽  
Microtubule Motor ◽  
Discrete Domains

AbstractHypertension, exercise, and pregnancy are common triggers of cardiac remodeling, which occurs primarily through the hypertrophy of individual cardiomyocytes. During hypertrophy, stress-induced signal transduction increases cardiomyocyte transcription and translation, which promotes the addition of new contractile units through poorly understood mechanisms. The cardiomyocyte microtubule network is also implicated in hypertrophy, but via an unknown role. Here, we show that microtubules are indispensable for cardiac growth via spatiotemporal control of the translational machinery. We find that the microtubule motor Kinesin-1 distributes mRNAs and ribosomes along microtubule tracks to discrete domains within the cardiomyocyte. Upon hypertrophic stimulation, microtubules redistribute mRNAs and new protein synthesis to sites of growth at the cell periphery. If the microtubule network is disrupted, mRNAs and ribosomes collapse around the nucleus, which results in mislocalized protein synthesis, the rapid degradation of new proteins, and a failure of growth, despite normally increased translation rates. Together, these data indicate that mRNAs and ribosomes are actively transported to specific sites to facilitate local translation and assembly of contractile units, and suggest that properly localized translation – and not simply translation rate – is a critical determinant of cardiac hypertrophy. In this work, we find that microtubule based-transport is essential to couple augmented transcription and translation to productive cardiomyocyte growth during cardiac stress.

Placental insufficiency induces a sexually dimorphic response in the expression of cardiac growth and metabolic signalling molecules upon exposure to a postnatal western diet in guinea pigs

2021 ◽  
pp. 1-13
Author(s):  
Jack R.T. Darby ◽  
Jacky Chiu ◽  
Timothy R.H. Regnault ◽  
Janna L. Morrison
Keyword(s):  
Birth Weight ◽  
Mrna Expression ◽  
Female Offspring ◽  
Postnatal Life ◽  
Sexually Dimorphic ◽  
Fibrotic Response ◽  
Cardiac Growth ◽  
Signalling Molecules ◽  
Secondary Insult ◽  
Obesogenic Diet

Abstract There is a strong relationship between low birth weight (LBW) and an increased risk of developing cardiovascular disease (CVD). In postnatal life, LBW offspring are becoming more commonly exposed to the additional independent CVD risk factors, such as an obesogenic diet. However, how an already detrimentally programmed LBW myocardium responds to a secondary insult, such as an obesogenic diet (western diet; WD), during postnatal life is ill defined. Herein, we aimed to determine in a pre-clinical guinea pig model of CVD, both the independent and interactive effects of LBW and a postnatal WD on the molecular pathways that regulate cardiac growth and metabolism. Uterine artery ablation was used to induce placental insufficiency (PI) in pregnant guinea pigs to generate LBW offspring. Normal birth weight (NBW) and LBW offspring were weaned onto either a Control diet or WD. At ˜145 days after birth (young adulthood), male and female offspring were humanely killed, the heart weighed and left ventricle tissue collected. The mRNA expression of signalling molecules involved in a pathological hypertrophic and fibrotic response was increased in the myocardium of LBW male, but not female offspring, fed a WD as was the mRNA expression of transcription factors involved in fatty acid oxidation. The mRNA expression of glucose transporters was downregulated by LBW and WD in male, but not female hearts. This study has highlighted a sexually dimorphic cardiac pathological hypertrophic and fibrotic response to the secondary insult of postnatal WD consumption in LBW offspring.

Abstract 346: A Novel Interaction Between E2F and β-adrenergic Pathways Regulates Survival and Growth in Murine Myocardium

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Jennifer L Major ◽  
Maysoon Salih ◽  
Balwant S Tuana
Keyword(s):  
Protein Kinase ◽  
Left Ventricle ◽  
Fold Increase ◽  
Negative Regulator ◽  
P Value ◽  
Specific Expression ◽  
Cardiac Growth ◽  
Reduced Ejection Fraction ◽  
Hypertrophic Growth ◽  
Rb Pathway

The E2F/Pocket protein (Rb) pathway regulates cell growth, differentiation, and death by modulating gene expression. We previously examined this pathway in myocardium via manipulation of E2F6, which represses gene activity independently of Rb. Mice with cardiac specific expression of E2F6 develop dilated cardiomyopathy (DCM) without any signs of hypertrophic growth. We assessed the mechanisms of the apparent failure of compensatory growth as well as their response to the β-adrenergic agonist isoproterenol (iso). E2F6 transgenic (Tg) mice present with left ventricle dilation and significantly reduced ejection fraction as early as 2 weeks which persists into adulthood, but with no apparent increase in left ventricle weight: body weight (LVW:BW). E2F6-Tg mice treated with iso show double the increase in LVW: BW than their Wt counterparts (32% vs 16%, p-value: 0.007). Western blot revealed a specific activation of the β2-adrenergic pathway in Tg myocardium under basal conditions including a ~2-fold increase in β2-adrenergic receptors (β2-AR) (p-value: 8.9E-05), protein kinase A catalytic subunit (PKA-C) (p-value: 0.0176), activated c-SRC tyrosine-protein kinase (p-value: 0.0002), and an induction of the anti-apoptotic gene Bcl2. In contrast, a ~70% decrease in the cardiac growth regulator: AKT1 (p-value 0.0001) and a 4-fold increase in cyclic AMP dependent phosphodiesterase 4D (PDE4D), the negative regulator of PKA activity, was evident in Tg myocardium. The expression of E2F3 was de-regulated by E2F6, but was restored by iso while Rb expression was down-regulated. Thus deregulation of E2F/Rb pathway by E2F6 altered the β-adrenergic signaling pathway such that survival signaling was activated while hypertrophy was repressed resulting in the development of DCM without any increase in muscle mass. These data reveal a novel interplay between E2F and the β adrenergic pathway which regulate cardiac growth and fate.

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