A Biochemical and Morphological Study of Protein Synthesis in Normal Rat Myocardium

1969 ◽  
Vol 3 (1) ◽  
pp. 79-87 ◽  
Author(s):  
B. D. McCallister ◽  
A. L. Brown
Keyword(s):  
Protein Synthesis ◽  
Morphological Study ◽  
Rat Myocardium ◽  
Normal Rat

Differential expression of TNF-α, IL-6, and IGF-1 by graded mechanical stress in normal rat myocardium

2002 ◽  
Vol 282 (3) ◽  
pp. H926-H934 ◽  
Author(s):  
Emiliano A. Palmieri ◽  
Giulio Benincasa ◽  
Francesca Di Rella ◽  
Cosma Casaburi ◽  
Maria G. Monti ◽  
...  
Keyword(s):  
Time Course ◽  
De Novo ◽  
Mechanical Stretch ◽  
Progressive Increase ◽  
Compensatory Hypertrophy ◽  
Current Data ◽  
Rat Myocardium ◽  
Tnf Α ◽  
Normal Rat ◽  
Necrosis Factor

An isovolumic normal rat heart Langendorff model was used to examine the effects of moderate (15 mmHg) and severe (35 mmHg) mechanical stretch on the time course (from 0 to 60 min) of myocardial expression of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and insulin-like growth factor (IGF)-1 and their cognate receptors. After 10 min of moderate stretch, TNF-α was de novo expressed, whereas constitutive IL-6 and IGF-1 levels were slightly upregulated; no further changes occurred up to 60 min. In comparison, severe stretch resulted in a higher and progressive increase in TNF-α, IL-6, and IGF-1 expression up to 20 min. After 20 min, whereas TNF-α expression further increased, IL-6 and IGF-1 levels progressively reduced to values lower than those observed under moderate stretch and in unstretched (5 mmHg) control myocardium (IL-6). Mechanical stretch did not significantly alter the expression of the cognate receptors. Indeed, the TNF-α receptor (p55) tended to be progressively upregulated under severe stretch over time. The current data provide the first demonstration that TNF-α, IL-6, and IGF-1 ligand-receptor systems are differentially expressed within the normal rat myocardium in response to graded mechanical stretch. Such findings may have potential implications with regard to compensatory hypertrophy and failure.

Regulation by thyroid status of c-myc, c-fos and H-ras mRNAs in the rat myocardium

1991 ◽  
Vol 130 (2) ◽  
pp. 239-244 ◽  
Author(s):  
N. K. Green ◽  
M. D. Gammage ◽  
J. A. Franklyn ◽  
M. C. Sheppard
Keyword(s):  
Protein Synthesis ◽  
Thyroid Hormones ◽  
Contractile Protein ◽  
Rat Myocardium ◽  
Direct Effects ◽  
Thyroid Status ◽  
Critical Signal ◽  
Ras Genes ◽  
Intracellular Signals ◽  
Oncogene Products

ABSTRACT Effects of thyroid status on expression of a variety of myocardial genes, such as those encoding contractile proteins, have been reported, as well as interactions between thyroid hormones and developmental and haemodynamic regulation of contractile protein synthesis. In addition, it is clear that developmental and haemodynamic factors regulate expression of specific proto-oncogenes, including c-myc, c-fos and H-ras, in the myocardium but the effect of thyroid status on such proto-oncogene products, which are proposed to play a critical signal-transducing role in the heart, has been previously unexplored. In order to determine whether changes in thyroid status are associated with changes in expression of these putative intracellular signals, we examined the effect of hypothyroidism and tri-iodothyronine (T3) treatment on myocardial levels of c-myc, c-fos and H-ras mRNAs in the rat. The induction of hypothyroidism was associated with a marked increase in myocardial c-myc, c-fos and H-ras mRNAs, changes reversed by 72 h of T3 replacement. Administration of T3 to euthyroid rats had no significant effect on myocardial c-myc or c-fos mRNAs, but inhibition of H-ras mRNA by T3 was evident. These observations demonstrating influences of thyroid status on expression of specific proto-oncogenes suggest that thyroid hormones, as well as exerting direct effects on expression of functionally important myocardial genes, also interact with the cellular transduction pathways mediated by the products of the c-myc, c-fos and H-ras genes. Journal of Endocrinology (1991) 130, 239–244

CONCERNING THE INFLUENCE OF HALOTHANE AND CHLOROFORM ON PROTEIN SYNTHESIS IN ACTIVATED AND NORMAL RAT LIVER

1969 ◽  
Vol 13 (2) ◽  
pp. 180
Author(s):  
K. L. SCHOLLER ◽  
E. M??LLER ◽  
U. V. PLEHWE ◽  
ROBERT W. VIRTUE
Keyword(s):  
Protein Synthesis ◽  
Rat Liver ◽  
Normal Rat

Mibefradil Improves β-drenergic Responsiveness and Intracellular Ca2+ Handling in Hypertrophied Rat Myocardium

2002 ◽  
Vol 227 (5) ◽  
pp. 336-344 ◽  
Author(s):  
Jiang-Yong Min ◽  
Achim Meissner ◽  
Jianan Wang ◽  
James P. Morgan
Keyword(s):  
Isometric Contraction ◽  
Positive Inotropic Effect ◽  
Channel Blocker ◽  
Contractile Response ◽  
Papillary Muscles ◽  
Rat Myocardium ◽  
Adrenergic Stimulation ◽  
Hypertrophied Myocardium ◽  
Prolonged Duration ◽  
Normal Rat

The present study investigated the effects of mibefradil, a novel T-type channel blocker, on ventricular function and intracellular Ca2+ handling in normal and hypertrophied rat myocardium. Ca2+ transient was measured with the biolumlnescent protein, aequorin. Mibefradil (2 μM) produced nonsignificant changes in isometric contraction and peak systolic intracellular Ca2+ concentration ([Ca2+],) in normal rat myocardium. Hypertrophied papillary muscles isolated from aortic-banded rats 10 weeks after operation demonstrated a prolonged duration of isometric contraction, as well as decreased amplitudes of developed tension and peak Ca2+ transient compared with the sham-operated group. Additionally, diastolic [Ca2+], Increased In hypertrophied rat myocardium. The positive inotropic effect of isoproterenol stimulation was blunted in hypertrophied muscles despite a large increase in Ca2+ transient amplitude. Afterglimmers and corresponding aftercontractions were provoked with isoproterenol (10-5 and 10-4 M) stimulation in 4 out of 16 hypertrophied muscles, but were eliminated in the presence of mibefradil (2 μM). In addition, hypertrophied muscles in the presence of mibefradil had a significant improvement of contractile response to isoproterenol stimulation and a reduced diastolic [Ca2+], although a mild decrease of peak Ca2+-transient was also shown. However, verapamil (2 μM) did not restore the inotropic and Ca2+ modulating effects of isoproterenol in hypertrophied myocardium. Mibefradil partly restores the positive Inotropic response to β-adrenergic stimulation in hypertrophied myocardium from aortic-banded rats, an effect that might be useful in hypertrophied myocardium with impaired [Ca2+], homeostasis.

scholarly journals Transmural gradients of preferential diffusion motility in the normal rat myocardium characterized by diffusion tensor imaging

2015 ◽  
Vol 17 (S1) ◽  
Author(s):  
Archontis Giannakidis ◽  
Pedro Ferreira ◽  
Grant T Gullberg ◽  
David Firmin ◽  
Dudley J Pennell
Keyword(s):  
Diffusion Tensor Imaging ◽  
Diffusion Tensor ◽  
Rat Myocardium ◽  
Preferential Diffusion ◽  
Normal Rat

Calcineurin is required for protein synthesis by normal rat pancreatic acini

2000 ◽  
Vol 118 (4) ◽  
pp. A158 ◽  
Author(s):  
Maria-Dolors Sans ◽  
John A. Williams
Keyword(s):  
Protein Synthesis ◽  
Pancreatic Acini ◽  
Normal Rat

scholarly journals ALTERATIONS IN POLYRIBOSOMES DURING ERYTHROID CELL MATURATION

1964 ◽  
Vol 22 (3) ◽  
pp. 599-611 ◽  
Author(s):  
Richard A. Rifkind ◽  
David Danon ◽  
Paul A. Marks
Keyword(s):  
Protein Synthesis ◽  
Quantitative Analysis ◽  
Morphological Study ◽  
Protein Biosynthesis ◽  
Cell Maturation ◽  
Erythroid Cell ◽  
Erythroid Cells ◽  
The Stability

This communication presents a morphological study of the changes in ribosome content and organization which occur during the maturation of erythroid cells of the phenylhydrazine-treated rabbit. Electron micrographs of thin sectioned nucleated and non-nucleated erythroid cells have been subjected to a quantitative analysis of the distribution of ribosomes as polyribosomes of various sizes and as single ribosomes. The ribosomes of nucleated erythroid cells of marrow are virtually all arranged in the polyribosome configuration consisting of clusters of 2 to 6 individual ribosomes. These cells are the most active in the erythroid series in protein biosynthesis. During maturation to the non-nucleated reticulocyte stage, found in the circulating blood, there is a decrease in protein synthesizing capacity, a fall in total ribosome content, and, more significantly, a decrease in the number and size of polyribosomes. Maturation to the ribosome-free erythrocyte, either under in vitro or in vivo conditions, entails a further decrease in protein synthesis which correlates with a progressive disaggregation of the biosynthetically active polyribosomes into smaller clusters and inactive single ribosomes. Possible models which may account for the stability of the polyribosome and for the mechanism of polyribosome dissociation are discussed.

Abstract 275: Electrophysiological Consequences of AAV9 mediated SERCA2a Gene Transfer to Normal Rat Myocardium

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Chaoqin Xie ◽  
Dongtak Jeong ◽  
Erik Kohlbrenner ◽  
Roger J Hajjar ◽  
Fadi G Akar
Keyword(s):  
Gene Transfer ◽  
Ex Vivo ◽  
Preventive Therapy ◽  
Low Flow ◽  
Rat Myocardium ◽  
Tail Vein Injection ◽  
Rat Hearts ◽  
Normal Rat ◽  
End Stage Heart Failure ◽  
End Stage

SERCA2a gene transfer to the failing heart improves its mechanical function and inhibits arrhythmic triggers caused by aberrant calcium waves. The majority of arrhythmias occur before onset of end-stage heart failure when SR function is not compromised. Examination of the electrophysiological (EP) consequences of SERCA2a gene therapy in normal hearts is imperative in determining its potential toxicity as a preventive therapy during early stages of remodeling. We hypothesized that AAV9 mediated gene transfer of SERCA2a to normal rat hearts may promote the incidence of arrhythmic triggers under conditions of intracellular calcium (Ca2+) overload. Methods: Rats underwent tail vein injection of 5x10E11vg AAV9.SERCA2a (N=8) or AAV9.GFP (N=3). 6 naïve uninjected rats served as controls (Ctl). Using high resolution optical action potential (AP) imaging, we characterized the EP substrate 6 weeks post gene transfer. Ex vivo hearts were examined during normoxic perfusion and challenge with low flow ischemia for 1h followed by reperfusion. Arrhythmia susceptibility was determined under conditions of Ca2+ overload. Results: Surprisingly, AAV9.GFP hearts exhibited markedly prolonged AP durations (APD) and slower conduction velocities (CV) compared to AAV9.SERCA2a and Ctl hearts. Challenge of AAV9.GFP but not AAV9.SERCA2a or Ctl hearts with burst pacing always resulted in VF. Remarkably, APD & CV rate relationships were identical in Ctl and AAV9.SERCA2a hearts (p=NS). Elevation of pacing rate resulted in a comparable level of AP alternans followed by loss of 1:1 capture in both groups. No evidence of triggered APs was found in AAV9.SERCA2a or Ctl hearts in response to burst stimulation. Ischemia for 1hr produced comparable changes in APD and CV. Challenge with burst stimuli during ischemia elicited arrhythmias in 2/6 Ctl and 6/8 AAV9.SERCA2a hearts (p=0.277, NS). Upon reperfusion, 1/4 & 0/2 remaining Ctl and AAV9.SERCA2a hearts exhibited VF. Conclusion: Surprisingly, AAV9.GFP but not AAV9.SERCA2a gene transfer to normal rat myocardium alters EP properties and promotes Ca2+ mediated arrhythmias. Lack of an EP phenotype of AAV9.SERCA2a suggests an upper limit of endogenous SERCA2a expression in normal rodent myocardium that is not exceeded by gene transfer.

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