Hypertrophic growth

Cardiac hypertrophy is a growth process that occurs in response to stress stimuli or injury, and leads to the induction of several pathways to alter gene expression. Under hypertrophic stimuli, sarcomeric structure is disrupted, both as a consequence of gene expression and local changes in sarcomeric proteins. Cardiac-restricted ankyrin repeat protein (CARP) is one such protein that function both in cardiac sarcomeres and at the transcriptional level. We postulate that due to this dual nature, CARP plays a key role in maintaining the cardiac sarcomere. GATA4 is another protein detected in cardiomyocytes as important in hypertrophy, as it is activated by hypertrophic stimuli, and directly binds to DNA to alter gene expression. Results of GATA4 activation over time were inconclusive; however, the role of CARP in mediating hypertrophic growth in cardiomyocytes was clearly demonstrated. In this study, Neonatal Rat Ventricular Myocytes were used as a model to detect changes over time in CARP and GATA4 under hypertrophic stimulation by phenylephrine and high serum media. Results were detected by analysis of immunoblotting. The specific role that CARP plays in mediating cellular growth under hypertrophic stimuli was studied through immunofluorescence, which demonstrated that cardiomyocyte growth with hypertrophic stimulation was significantly blunted when NRVMs were co-treated with CARP siRNA. These data suggest that CARP plays an important role in the hypertrophic response in cardiomyocytes.

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Tumor Necrosis Factor-α Provokes a Hypertrophic Growth Response in Adult Cardiac Myocytes

Circulation ◽

10.1161/01.cir.95.5.1247 ◽

1997 ◽

Vol 95 (5) ◽

pp. 1247-1252 ◽

Cited By ~ 208

Author(s):

Tomoyuki Yokoyama ◽

Masayuki Nakano ◽

John L. Bednarczyk ◽

Bradley W. McIntyre ◽

Mark Entman ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Cardiac Myocytes ◽

Tumor Necrosis ◽

Growth Response ◽

Tumor Necrosis Factor Α ◽

Hypertrophic Growth ◽

Adult Cardiac Myocytes ◽

Factor Α ◽

Necrosis Factor

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Heart failure—emerging roles for the mitochondrial pyruvate carrier

Cell Death and Differentiation ◽

10.1038/s41418-020-00729-0 ◽

2021 ◽

Author(s):

Mariana Fernandez-Caggiano ◽

Philip Eaton

Keyword(s):

Heart Failure ◽

Warburg Effect ◽

Translational Regulation ◽

Hypertrophic Growth ◽

Metabolic Adaptations ◽

Mitochondrial Pyruvate Carrier ◽

Heart Failure Progression ◽

Mitochondrial Oxidation ◽

Human And Mouse ◽

The Warburg Effect

AbstractThe mitochondrial pyruvate carrier (MPC) is the entry point for the glycolytic end-product pyruvate to the mitochondria. MPC activity, which is controlled by its abundance and post-translational regulation, determines whether pyruvate is oxidised in the mitochondria or metabolised in the cytosol. MPC serves as a crucial metabolic branch point that determines the fate of pyruvate in the cell, enabling metabolic adaptations during health, such as exercise, or as a result of disease. Decreased MPC expression in several cancers limits the mitochondrial oxidation of pyruvate and contributes to lactate accumulation in the cytosol, highlighting its role as a contributing, causal mediator of the Warburg effect. Pyruvate is handled similarly in the failing heart where a large proportion of it is reduced to lactate in the cytosol instead of being fully oxidised in the mitochondria. Several recent studies have found that the MPC abundance was also reduced in failing human and mouse hearts that were characterised by maladaptive hypertrophic growth, emulating the anabolic scenario observed in some cancer cells. In this review we discuss the evidence implicating the MPC as an important, perhaps causal, mediator of heart failure progression.

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Processed By-Products from Soy Beverage (Okara) as Sustainable Ingredients for Nile Tilapia (O. niloticus) Juveniles: Effects on Nutrient Utilization and Muscle Quality

Animals ◽

10.3390/ani11030590 ◽

2021 ◽

Vol 11 (3) ◽

pp. 590

Author(s):

Glenise B. Voss ◽

Vera Sousa ◽

Paulo Rema ◽

Manuela. E. Pintado ◽

Luísa M. P. Valente

Keyword(s):

Nile Tilapia ◽

Lactobacillus Rhamnosus ◽

Protein Digestibility ◽

Nutrient Utilization ◽

Nutrient Digestibility ◽

Fish Growth ◽

Muscle Quality ◽

Whole Body ◽

Hypertrophic Growth ◽

Bifidobacterium Animalis

The apparent digestibility coefficients (ADCs) of differently processed okara meals were assessed in Nile tilapia diets: dried okara not autoclaved (FOK), dried okara autoclaved (AOK), okara hydrolyzed with Alcalase (ALOK) or Cynara cardunculus proteases (CYOK), and hydrolyzed okara fermented with lactic bacteria: Lactobacillus rhamnosus R11 (CYR11OK) or Bifidobacterium animalis ssp. lactis Bb12 (CYB12OK). Okara processing significantly affected nutrient digestibility: dry matter ADC was highest in CYR11OK (80%) and lowest in FOK (40%). The lowest protein digestibility was observed in CYR11OK (72%), and the highest in AOK (97%) and CYOK (91%), evidencing the effectiveness of the autoclave and the use of C. cardunculus proteases to increase okara protein bioavailability. The inclusion of up to 20% of AOK or CYOK did not affect fish growth, nutrient utilization, or whole body composition of Nile tilapia. The flesh quality (color, pH, water activity, cohesiveness, elasticity and resilience) was not affected by the dietary incorporation of AOK or CYOK. Fish fed with AOK diets stand out for their high density of muscle fibers, particularly in AOK20, which can explain their high muscle firmness and may result in further hypertrophic growth. Altogether, results suggest that hydrolyzed or autoclaved okara are valuable ingredients for Nile tilapia diets.

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Pathogenic Microenvironment from Diabetic–Obese Visceral and Subcutaneous Adipocytes Activating Differentiation of Human Healthy Preadipocytes Increases Intracellular Fat, Effect of the Apocarotenoid Crocetin

Nutrients ◽

10.3390/nu13031032 ◽

2021 ◽

Vol 13 (3) ◽

pp. 1032

Author(s):

Lesgui Alviz ◽

David Tebar-García ◽

Raquel Lopez-Rosa ◽

Eva M. Galan-Moya ◽

Natalia Moratalla-López ◽

...

Keyword(s):

Adipose Tissue ◽

Subcutaneous Adipose Tissue ◽

Bioactive Components ◽

Hypertrophic Growth ◽

Visceral Adipose ◽

Subcutaneous Adipose ◽

Oil Red O Staining ◽

Oil Red O ◽

Excessive Accumulation

In diabetes mellitus type 2 (DM2), developed obesity is referred to as diabesity. Implementation of a healthy diet, such as the Mediterranean, prevents diabesity. Saffron is frequently used in this diet because of its bioactive components, such as crocetin (CCT), exhibit healthful properties. It is well known that obesity, defined as an excessive accumulation of fat, leads to cardiometabolic pathology through adiposopathy or hypertrophic growth of adipose tissue (AT).This is related to an impaired adipogenic process or death of adipocytes by obesogenic signals. We aimed to evaluate the effect of the pathogenic microenvironment and CCT, activating differentiation of healthy preadipocytes (PA). For this, we used human cryopreserved PA from visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) depots obtained from healthy and obese-DM2 donors. We studied the effect of a metabolically detrimental (diabesogenic) environment, generated by obese-DM2 adipocytes from VAT (VdDM) or SAT (SdDM), on the viability and accumulation of intracellular fat of adipocytes differentiated from healthy PA, in the presence or absence of CCT (1 or 10 μM). Intracellular fat was quantified by Oil Red O staining. Cytotoxicity was measured using the MTT assay. Our results showed that diabesogenic conditions induce cytotoxicity and provide a proadipogenic environment only for visceral PA. CCT at 10 μM acted as an antiadipogenic and cytoprotective compound.

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Microtubule-dependent distribution of mRNA in adult cardiocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01275.2007 ◽

2008 ◽

Vol 294 (3) ◽

pp. H1135-H1144 ◽

Cited By ~ 17

Author(s):

Dimitri Scholz ◽

Catalin F. Baicu ◽

William J. Tuxworth ◽

Lin Xu ◽

Harinath Kasiganesan ◽

...

Keyword(s):

Protein Synthesis ◽

Fluorescent Protein ◽

Average Distance ◽

Yellow Fluorescent Protein ◽

Pressure Overload ◽

Structural Protein ◽

Protein Fusion ◽

Microtubule Depolymerization ◽

Microtubule Network ◽

Hypertrophic Growth

Synthesis of myofibrillar proteins in the diffusion-restricted adult cardiocyte requires microtubule-based active transport of mRNAs as part of messenger ribonucleoprotein particles (mRNPs) to translation sites adjacent to nascent myofibrils. This is especially important for compensatory hypertrophy in response to hemodynamic overloading. The hypothesis tested here is that excessive microtubule decoration by microtubule-associated protein 4 (MAP4) after cardiac pressure overloading could disrupt mRNP transport and thus hypertrophic growth. MAP4-overexpressing and pressure-overload hypertrophied adult feline cardiocytes were infected with an adenovirus encoding zipcode-binding protein 1-enhanced yellow fluorescent protein fusion protein, which is incorporated into mRNPs, to allow imaging of these particles. Speed and distance of particle movement were measured via time-lapse microscopy. Microtubule depolymerization was used to study microtubule-based transport and distribution of mRNPs. Protein synthesis was assessed as radioautographic incorporation of [3H]phenylalanine. After microtubule depolymerization, mRNPs persist only perinuclearly and apparent mRNP production and protein synthesis decrease. Reestablishing microtubules restores mRNP production and transport as well as protein synthesis. MAP4 overdecoration of microtubules via adenovirus infection in vitro or following pressure overloading in vivo reduces the speed and average distance of mRNP movement. Thus cardiocyte microtubules are required for mRNP transport and structural protein synthesis, and MAP4 decoration of microtubules, whether directly imposed or accompanying pressure-overload hypertrophy, causes disruption of mRNP transport and protein synthesis. The dense, highly MAP4-decorated microtubule network seen in severe pressure-overload hypertrophy both may cause contractile dysfunction and, perhaps even more importantly, may prevent a fully compensatory growth response to hemodynamic overloading.

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Increased expression of UBF is a critical determinant for rRNA synthesis and hypertrophic growth of cardiac myocytes

The FASEB Journal ◽

10.1096/fj.01-0853fje ◽

2001 ◽

Cited By ~ 4

Author(s):

Y. Brandenburger

Keyword(s):

Cardiac Myocytes ◽

Rrna Synthesis ◽

Critical Determinant ◽

Hypertrophic Growth

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Activation of NF- B is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.111155798 ◽

2001 ◽

Vol 98 (12) ◽

pp. 6668-6673 ◽

Cited By ~ 237

Author(s):

N. H. Purcell ◽

G. Tang ◽

C. Yu ◽

F. Mercurio ◽

J. A. DiDonato ◽

...

Keyword(s):

Hypertrophic Growth ◽

Ventricular Cardiomyocytes

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The c-myc proto-oncogene regulates cardiac development in transgenic mice.

Molecular and Cellular Biology ◽

10.1128/mcb.10.7.3709 ◽

1990 ◽

Vol 10 (7) ◽

pp. 3709-3716 ◽

Cited By ~ 128

Author(s):

T Jackson ◽

M F Allard ◽

C M Sreenan ◽

L K Doss ◽

S P Bishop ◽

...

Keyword(s):

Transgenic Mice ◽

Mrna Expression ◽

Cardiac Myocyte ◽

Cellular Proliferation ◽

Cardiac Development ◽

Constitutive Expression ◽

Transgenic Animals ◽

Hypertrophic Growth ◽

Myocyte Proliferation

During the maturation of the cardiac myocyte, a transition occurs from hyperplastic to hypertrophic growth. The factors that control this transition in the developing heart are unknown. Proto-oncogenes such as c-myc have been implicated in the regulation of cellular proliferation and differentiation, and in the heart the switch from myocyte proliferation to terminal differentiation is synchronous with a decrease in c-myc mRNA abundance. To determine whether c-myc can influence myocyte proliferation or differentiation, we examined the in vivo effect of increasing c-myc expression during embryogenesis and of preventing the decrease in c-myc mRNA expression that normally occurs during cardiac development. The model system used was a strain of transgenic mice exhibiting constitutive expression of c-myc mRNA in cardiac myocytes throughout development. In these transgenic mice, increased c-myc mRNA expression was found to be associated with both atrial and ventricular enlargement. This increase in cardiac mass was secondary to myocyte hyperplasia, with the transgenic hearts containing more than twice as many myocytes as did nontransgenic hearts. The results suggest that in the transgenic animals there is additional hyperplastic growth during fetal development. However, this additional proliferative growth is not reflected in abnormal myocyte maturation, as assessed by the expression of the cardiac and skeletal isoforms of alpha-actin. The results of this study indicate that constitutive expression of c-myc mRNA in the heart during development results in enhanced hyperplastic growth and suggest a regulatory role for this proto-oncogene in cardiac myogenesis.

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