Expression and cellular distribution of heat-shock and nuclear oncogene proteins in rat hearts

1991 ◽  
Vol 261 (5) ◽  
pp. H1443-H1451 ◽  
Author(s):  
L. H. Snoeckx ◽  
F. Contard ◽  
J. L. Samuel ◽  
F. Marotte ◽  
L. Rappaport
Keyword(s):  
Heat Shock ◽  
Cardiac Development ◽  
Pressure Overload ◽  
Adult Rats ◽  
Coronary Smooth Muscle ◽  
Rat Hearts ◽  
Nonmuscle Cells ◽  
Ontogenic Development ◽  
Coronary Endothelium ◽  
Myocardial Muscle

An early, transient accumulation of mRNAs of the protooncogenes c-fos and c-myc and the heat-shock protein HSP70 has been described in hypertrophying rat hearts. It is unclear 1) in which cardiac cell type-these gene activations occur and 2) whether the corresponding proteins are translated. We studied protein expression in rat hearts during ontogenic development and under stress conditions associated with pressure overload with the use of immunofluorescent techniques. During cardiac development no HSP70 could be detected. c-Fos was expressed consistently after birth but only in coronary smooth muscle cells, and c-Myc was found exclusively in adult coronary endothelium and myocardial nonmuscle cells. In adult rats, HSP70 and, to a lesser extent, c-Fos were induced in myocardial muscle and some nonmuscle cells within 3 h following methohexital sodium anesthesia. A similar, more intense immunolabeling of these peptides was observed after thoracotomy and/or aortic stenosis. The coronary c-Fos and c-Myc labeling remained unchanged in these conditions. Thus the expression in cardiac muscle and nonmuscle cells of the three peptides differs and depends on different triggers.

scholarly journals Speckle tracking echocardiography could detect the difference of pressure overload-induced myocardial remodelling between young and adult rats

2020 ◽  
Vol 17 (163) ◽  
pp. 20190808 ◽  
Author(s):  
Pei Niu ◽  
Li Li ◽  
Zhongjie Yin ◽  
Jie Du ◽  
Wenchang Tan ◽  
...  
Keyword(s):  
Speckle Tracking ◽  
Speckle Tracking Echocardiography ◽  
Strain Analysis ◽  
Pressure Overload ◽  
Free Wall ◽  
Adult Rats ◽  
Adult Rat ◽  
Rat Hearts ◽  
Myocardial Remodelling ◽  
The Difference

The assessment by speckle tracking echocardiography (STE) provides useful information on regional and global left ventricular (LV) functions. The aim of the study is to investigate if STE-based strain analysis could detect the difference of pressure overload-induced myocardial remodelling between young and adult rats. Physiological, haemodynamic, histological measurements were performed post-operatively in young and adult rats with transverse aortic constriction (TAC) as well as the age-matched shams. Two-way ANOVA was used to detect the statistical difference of various measured parameters. Pressure overload decreased the ejection fraction, fractional shortening, d p /d t max and | d p / d t min | , but increased the LV end-diastolic (ED) pressure in adult rat hearts for nine weeks after TAC operation than those in young rat hearts. Pressure overload also resulted in different changes of peak strain and strain rate in the free wall, but similar changes in the interventricular septum of young and adult rat hearts. The changes in myocardial remodelling were confirmed by the histological analysis including the increased apoptosis rate of myocytes and collagen area ratio in the free wall of adult rat hearts of LV hypertrophy when compared with the young. Pressure overload alters myocardial components in different degrees between young and adult animals. STE-based strain analysis could detect the subtle difference of pressure overload-induced myocardial remodelling between young and adult rats.

Isomyosin and thyroid hormone levels in pressure-overloaded weanling and adult rat hearts

1985 ◽  
Vol 248 (3) ◽  
pp. H305-H310 ◽  
Author(s):  
A. F. Martin ◽  
D. C. Robinson ◽  
R. T. Dowell
Keyword(s):  
Pressure Overload ◽  
Adult Rats ◽  
Adult Rat ◽  
Rat Hearts ◽  
Weanling Rats ◽  
Significant Difference ◽  
Thyroid Hormone Levels ◽  
The Right ◽  
The Relationship ◽  
Cardiac Enlargement

We examined the relationship between ventricular isomyosin composition and plasma thyroxine (T4) 5 wk after partial constriction of the abdominal aorta in weanling (21 day) and adult (8 wk) rats. Cardiac enlargement in weanling aorta-constricted animals was associated with a significant (P less than 0.001) decrease in %V1 isomyosin in both left (32%) and right ventricles (25%) with a corresponding increase in the %V3 isomyosin and a reduction in plasma T4 levels. However, the ratio of V1/T4 was similar in weanling control (17.8 +/- 0.8) and aorta-constricted (18.0 +/- 1.4) rats. In adult aorta-constricted animals, there was a significant (P less than 0.001) reduction in the %V1 (16%) isomyosin in the left ventricle and a smaller decrease in the right ventricular V1 (8%) with no change in plasma T4 levels. There was also a significant difference in V1/T4 between control (16.1 +/- 0.4) and aorta-constricted (13.9 +/- 0.7) adult rats in contrast to the maintenance of the V1/T4 in weanling aorta-constricted animals. Thus both increased workload and changes in thyroxine levels contribute to the isomyosin redistribution seen in weanling rats subjected to a pressure overload, whereas, in adult hypertrophied hearts, alterations of the ventricular isomyosin composition appear to be due solely to the increased pressure overload.

scholarly journals Localization and partial characterization of ADP-ribosylation products in hearts from adult and neonatal rats

1990 ◽  
Vol 270 (3) ◽  
pp. 591-597 ◽  
Author(s):  
K J Piron ◽  
K K McMahon
Keyword(s):  
Rat Heart ◽  
Cardiac Development ◽  
Neonatal Rat ◽  
Nuclear Fraction ◽  
Adult Rats ◽  
Adp Ribosylation ◽  
Adult Rat ◽  
Snake Venom Phosphodiesterase ◽  
Rat Hearts ◽  
Neonatal Rat Heart

The subcellular distributions of endogenous ADP-ribosylation products in hearts from 1-day-old neonatal and adult rats were investigated. In adult rat heart a 52 kDa mono-ADP-ribosylation product was identified in the plasma membrane fraction. In contrast, in neonatal rat heart a 130 kDa poly-ADP-ribosylation product was present in the nuclear fraction. The monomeric and polymeric nature of the two ADP-ribosylation products was determined by their sensitivity to thymidine and by analysis of their snake venom phosphodiesterase products. NADP+ enhanced both the mono- and polymeric reactions. The ADP-ribose-protein linkage of the adult 52 kDa product was stable to 1 h of treatment with hydroxylamine (0.5 M) and mercury ions, but was sensitive to alkali and a 12 h treatment with hydroxylamine (1 M). This is suggestive of an arginine linkage. The 130 kDa poly-ADP-ribosylation product from the neonatal rat heart was alkalilabile but stable to both hydroxylamine and HgCl2. This implies the presence of an unusual linkage in the 130 kDa product. The presence of these different ADP-ribosylation products in adult and neonatal rat hearts suggests the possible importance of these proteins and their ADP-ribosylation during cardiac development.

The complex network of mTOR signalling in the heart

2021 ◽  
Author(s):  
Sebastiano Sciarretta ◽  
Maurizio Forte ◽  
Giacomo Frati ◽  
Junichi Sadoshima
Keyword(s):  
Cardiovascular System ◽  
Cardiac Development ◽  
Metabolic Stress ◽  
Pressure Overload ◽  
Current Data ◽  
Loss Of Function ◽  
Extracellular Signals ◽  
Mtorc1 Activation ◽  
Mtor Modulation ◽  
Mtor Signalling

Abstract The mechanistic target of rapamycin (mTOR) integrates several intracellular and extracellular signals involved in the regulation of anabolic and catabolic processes. mTOR assembles into two macromolecular complexes, named mTORC1 and mTORC2, which have different regulators, substrates and functions. Studies of gain- and loss-of-function animal models of mTOR signalling revealed that mTORC1/2 elicits both adaptive and maladaptive functions in the cardiovascular system. Both mTORC1 and mTORC2 are indispensable for driving cardiac development and cardiac adaption to stress, such as pressure overload. However, persistent and deregulated mTORC1 activation in the heart is detrimental during stress and contributes to the development and progression of cardiac remodelling and genetic and metabolic cardiomyopathies. In this review, we discuss the latest findings regarding the role of mTOR in the cardiovascular system, both under basal conditions and during stress, such as pressure overload, ischemia, and metabolic stress. Current data suggest that mTOR modulation may represent a potential therapeutic strategy for the treatment of cardiac diseases.

Prior treatment with heat shock attenuates the stress response in isolated working rat hearts

1995 ◽  
Vol 73 (1-2) ◽  
pp. 31-39
Author(s):  
Todd A. Dakin ◽  
R. William Currie
Keyword(s):  
Heat Shock ◽  
Control Mechanism ◽  
Negative Control ◽  
Northern Analysis ◽  
Moderate Increase ◽  
Flow Rates ◽  
Rat Hearts ◽  
Heart Perfusion ◽  
Paired Control ◽  
Working Heart

We examined the expression of the mRNAs encoding for the inducible heat shock protein (HSP) 71 and the constitutively synthesized HSP73 in control and 24-h post-heat-shocked (post-HS) hearts during isolated working heart perfusion. Paired control and 24-h post-HS rat hearts were perfused in the working heart mode for 1, 2, 3, or 4 h. Aortic and coronary flow rates and heart rates were not different between the control and 24-h post-HS hearts during the perfusion periods. After perfusion, total RN A was extracted and separated by gel electrophoresis. RNA was blotted to membranes, subsequently probed with 32P-labelled cDNA probes for HSP71 and HSP73 transcripts, and autoradiographed. Control hearts showed a sharp increase in transcripts for HSP71 and a more moderate increase in transcripts for HSP73 accumulation during perfusion. However, the increase in HSP71 and HSP73 transcripts in the HS hearts was markedly less than that in the control hearts. This suppression in gene expression in the HS hearts seems to suggest a negative control mechanism regulating transcription of mRNA encoding HSP71 and HSP73.Key words: mRNA, heart, Northern analysis, working heart perfusion, heat shock.

Abstract 791: A Critical Role for Bmper (BMP-binding Endothelial cell precursor-derived Regulator) in Cardiac Muscle Mass Regulation during Development and Pressure Overload Induced Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monte Willis ◽  
Rongqin Ren ◽  
Cam Patterson
Keyword(s):  
Cardiac Function ◽  
Cardiac Muscle ◽  
Muscle Mass ◽  
Cardiac Development ◽  
Critical Role ◽  
Pressure Overload ◽  
Posterior Wall ◽  
Fractional Shortening

Bone morphogenetic proteins (BMPs) of the TGF-beta superfamily, have been implicated in multiple processes during cardiac development. Our laboratory recently described an unprecedented role for Bmper in antagonizing BMP-2, BMP-4, and BMP-6. To determine the role of Bmper on cardiac development in vivo, we created Bmper null (Bmper −/−) mice by replacing exons 1 and 2 with GFP. Since Bmper −/− mice are perinatally lethal, we determined pre-natal cardiac function of Bmper −/− mice in utero just before birth. By echocardiography, E18.5 Bmper −/− embryos had decreased cardiac function (24.2 +/− 8.1% fractional shortening) compared to Bmper +/− and Bmper +/+ siblings (52.2 +/− 1.6% fractional shortening) (N=4/group). To further characterize the role of Bmper on cardiac function in adult mice, we performed echocardiography on 8-week old male and female Bmper +/− and littermate control Bmper +/+. Bmper +/− mice had an approximately 15% decrease in anterior and posterior wall thickness compared to sibling Bmper +/+ mice at baseline (n=10/group). Cross-sectional areas of Bmper +/− cardiomyocytes were approximately 20% less than wild type controls, indicating cardiomyocyte hypoplasia in adult Bmper +/− mice at baseline. Histologically, no significant differences were identified in representative H&E and trichrome stained adult Bmper +/− and Bmper +/+ cardiac sections at baseline. To determine the effects of Bmper expression on the development of cardiac hypertrophy, both Bmper +/− and Bmper +/+ sibling controls underwent transaortic constriction (TAC), followed by weekly echocardiography. While a deficit was identified in Bmper +/− mice at baseline, both anterior and posterior wall thicknesses increased after TAC, such that identical wall thicknesses were identified in Bmper +/− and Bmper +/+ mice 1–4 weeks after TAC. Notably, cardiac function (fractional shortening %) and histological evaluation revealed no differences between Bmper +/− and Bmper +/+ any time after TAC. These studies identify for the first time that Bmper expression plays a critical role in regulating cardiac muscle mass during development, and that Bmper regulates the development of hypertrophy in response to pressure overload in vivo.

Differential expression of alpha- and beta-enolase genes during rat heart development and hypertrophy

1995 ◽  
Vol 269 (6) ◽  
pp. H1843-H1851 ◽  
Author(s):  
A. Keller ◽  
J. D. Rouzeau ◽  
F. Farhadian ◽  
C. Wisnewsky ◽  
F. Marotte ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Development ◽  
Rat Heart ◽  
Cardiac Development ◽  
Transcript Level ◽  
Glycolytic Enzyme ◽  
High Ratio ◽  
Control Mechanisms ◽  
Nonmuscle Cells ◽  
A Minor

We have analyzed the transition between isoforms of the glycolytic enzyme enolase (2-phospho-D-glycerate hydrolyase; EC 4.2.1.11) in rat heart during normal and pathological growth. A striking fall in embryonic alpha-enolase gene expression occurs during cardiac development, mostly controlled at pretranslational steps. In fetal and neonatal hearts, muscle-specific beta-enolase gene expression is a minor contributor to total enolase. Control mechanisms of beta-enolase gene expression must include posttranscriptional steps. Aortic stenosis induces a rapid and drastic decrease in beta-enolase transcript level in cardiomyocytes, followed by the fall in beta-subunit level. In contrast, alpha-enolase transcript level is not significantly altered, although the corresponding subunit level increases in nonmuscle cells. We conclude that, like fetal heart, hypertrophic heart is characterized by a high ratio of alpha- to beta-enolase subunit concentrations. This study indicates that the decrease in beta-enolase gene expression may be linked to beneficial energetic changes in contractile properties occurring during cardiac hypertrophy

scholarly journals Adenylyl cyclase type 5 protein expression during cardiac development and stress

2009 ◽  
Vol 297 (5) ◽  
pp. H1776-H1782 ◽  
Author(s):  
Che-Lin Hu ◽  
Rachna Chandra ◽  
Hui Ge ◽  
Jayashree Pain ◽  
Lin Yan ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Adrenergic Receptor ◽  
Ventricular Hypertrophy ◽  
Cardiac Development ◽  
Mammalian Species ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Receptor Stimulation ◽  
Specific Antibodies ◽  
The Brain

Adenylyl cyclase (AC) types 5 and 6 (AC5 and AC6) are the two major AC isoforms expressed in the mammalian heart that mediate signals from β-adrenergic receptor stimulation. Because of the unavailability of isoform-specific antibodies, it is difficult to ascertain the expression levels of AC5 protein in the heart. Here we demonstrated the successful generation of an AC5 isoform-specific mouse monoclonal antibody and studied the expression of AC5 protein during cardiac development in different mammalian species. The specificity of the antibody was confirmed using heart and brain tissues from AC5 knockout mice and from transgenic mice overexpressing AC5. In mice, the AC5 protein was highest in the brain but was also detectable in all organs studied, including the heart, brain, lung, liver, stomach, kidney, skeletal muscle, and vascular tissues. Western blot analysis showed that AC5 was most abundant in the neonatal heart and declined to basal levels in the adult heart. AC5 protein increased in the heart with pressure-overload left ventricular hypertrophy. Thus this new AC5 antibody demonstrated that this AC isoform behaves similarly to fetal type genes, such as atrial natriuretic peptide; i.e., it declines with development and increases with pressure-overload hypertrophy.

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