Changes of Creatine Kinase Gene Expression in Rat Heart Post-Myocardial Infarction

1998 ◽  
Vol 30 (4) ◽  
pp. 803-810 ◽  
Author(s):  
Stefan Neubauer ◽  
Monika Frank ◽  
Kai Hu ◽  
Helga Remkes ◽  
Anne Laser ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Creatine Kinase ◽  
Rat Heart ◽  
Post Myocardial Infarction ◽  
Kinase Gene

Developmental regulation of creatine kinase gene expression by myogenic factors in embryonic mouse and chick skeletal muscle

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 1017-1029 ◽  
Author(s):  
G.E. Lyons ◽  
S. Muhlebach ◽  
A. Moser ◽  
R. Masood ◽  
B.M. Paterson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Striated Muscle ◽  
Myogenic Differentiation ◽  
Developmental Regulation ◽  
Specific Gene ◽  
Kinase Gene ◽  
Embryonic Mouse ◽  
Myogenic Factors

The B isoform of creatine kinase (BCK), which is expressed at a high level in embryonic neural tissues, is also expressed abundantly in developing striated muscle and is an early marker for skeletal myogenesis. Using isoform-specific 35S-labeled antisense cRNA probes for in situ hybridization, we have detected BCK mRNAs in embryonic mouse and chick myotomes, the first skeletal muscle masses to form in developing embryos. These transcripts are detectable as soon as myotomes are morphologically distinguishable. BCK is expressed at high levels in both skeletal and cardiac muscle in mouse and chick embryos. In the mouse, BCK transcript levels fall of rapidly in striated muscle shortly after the onset of MCK gene expression. The M isoform of creatine kinase (MCK), the striated muscle-specific isoform, is expressed later than BCK. In the mouse, BCK transcripts are expressed in myotomes at 8.5 days post coitum (p.c.), but MCK transcripts are not detected before 13 days p.c. In the chick, BCK mRNAs are present at Hamburger-Hamilton stage 13, but MCK mRNAs are not detected before stage 19. We have compared the patterns of expression of the CK genes with those of myogenic differentiation factor genes, which are thought to regulate skeletal muscle-specific gene expression. In the chick, both CMD1, first detected at stage 13, and myogenin, first detected at stage 15, are present prior to MCK, which begins to be expressed at stage 19. Unlike the mouse embryo, CMD1, the chick homologue of MyoD1, is expressed before chick myogenin. In the mouse, myogenin, first detected at 8.5 days p.c., is expressed at the same time as BCK in myotomes. Both myogenin and MyoD1, which begins to be detected two days later than myogenin, are expressed at least two days before MCK. It has been proposed that the myogenic factors, MyoD1 and myogenin, directly regulate MCK gene expression in the mouse by binding to its enhancer. However, our results show that MCK transcripts are not detected until well after MyoD1 and myogenin mRNAs are expressed, suggesting that these factors by themselves are not sufficient to initiate MCK gene expression.

Increased preproenkephalin A gene expression in the rat heart after induction of a myocardial infarction

1992 ◽  
Vol 70 (7) ◽  
pp. 593-598 ◽  
Author(s):  
Pierre Paradis ◽  
Michel Dumont ◽  
Pierre Bélichard ◽  
Jean-Lucien Rouleau ◽  
Simon Lemaire ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Coronary Artery ◽  
Relative Abundance ◽  
Rat Heart ◽  
Northern Blot Analysis ◽  
Time Intervals ◽  
Local Synthesis ◽  
Polysomal Fraction ◽  
Stimulation Of

The expression of preproenkephalin A (ppENK) gene was investigated in the rat heart, following the onset of myocardial infarction induced by ligation of the left anterior descending coronary artery. The relative abundance of ppENK mRNA and the level of enkephalins were measured by Northern blot analysis and radioimmunoassay, respectively, in the ventricles from control-unoperated, sham-operated, and operated rats. Three hours after the surgery, a comparison between rats with infarction and sham-operated rats revealed that the relative abundance of ppENK mRNA and the level of enkephalins were increased three- to four- and two- to three-fold, respectively, in the ventricles of rats with infarction. No difference was observed between rats with infarction and sham-operated rats 24 h after the surgery, or between rats with infarction compared at time intervals of 3 and 24 h following the surgery. The abundance of the ppENK mRNA in the polysomal fraction of the ventricular septum was also measured 3 h after the surgery and found to be threefold higher in rats with infarction as compared with sham-operated rats. These results indicate that the level of enkephalins rapidly increases in the ventricles of rats following myocardial infarction, and that this higher level may be ascribed to a stimulation of the local synthesis of enkephalins.Key words: preproenkephalin A, enkephalins, gene expression, myocardial infarction.

scholarly journals Acute changes of myocardial creatine kinase gene expression under β-adrenergic stimulation

2000 ◽  
Vol 1502 (3) ◽  
pp. 471-480 ◽  
Author(s):  
Stefan Hammerschmidt ◽  
Michael Bell ◽  
Nicole Büchler ◽  
Hans Wahn ◽  
Helga Remkes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Creatine Kinase ◽  
Adrenergic Stimulation ◽  
Kinase Gene ◽  
Acute Changes

scholarly journals Mitral valve leaflet response to ischemic mitral regurgitation: From gene expression to tissue remodeling

2019 ◽  
Author(s):  
Daniel P. Howsmon ◽  
Bruno V. Rego ◽  
Estibaliz Castillero ◽  
Salma Ayoub ◽  
Amir H. Khalighi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Extracellular Matrix ◽  
Mitral Valve ◽  
Mitral Regurgitation ◽  
Rna Sequencing ◽  
Immune Cells ◽  
Ischemic Mitral Regurgitation ◽  
Post Myocardial Infarction ◽  
Mechanical Anisotropy

AbstractAimsIschemic mitral regurgitation is frequently observed following myocardial infarction and is associated with higher mortality and poor clinical prognosis if left untreated. Accumulating evidence suggests that mitral valve leaflets actively remodel post–myocardial infarction, yet the cellular mechanisms underlying these responses and how this affects tissue function remain largely unknown. We sought to elucidate mitral valve remodeling post myocardial infarction at the tissue, cellular, and transcriptomic levels.Methods and ResultsThe mechanical behavior of ovine mitral valve leaflets pre– and 8 weeks post– myocardial infarction reveal a significant decrease in radial direction extensibility, which essentially eliminated the mechanical anisotropy typically observed in healthy mitral valves. Quantitative histology and ultrastructural assessment by transmission electron microscopy revealed altered leaflet composition and architecture at 8 weeks post–myocardial infarction. Assessment of the mitral valve interstitial cell nuclear aspect ratio, a metric of cellular deformation, revealed that they were on average rounder following myocardial infarction. RNA sequencing indicated that YAP-induced genes were elevated at 4 weeks post–myocardial infarction and genes related to extracellular matrix organization were some of the most downregulated in sheep with IMR compared to sheep without ischemic mitral regurgitation at 4 weeks post–myocardial infarction. Additionally, RNA sequencing revealed the possible recruitment of immune cells in this remodeling process due to the drastic elevation of CXCL9 and CLEC10A.ConclusionsOur multiscale assessment revealed significant mechanical and microstructural changes due to myocardial infarction. RNA sequencing provided a baseline for global gene expression changes in response to myocardial infarction with and without ischemic mitral regurgitation and suggests YAP-induced mechanotransduction, altered expression of extracellular matrix–related genes, and recruitment of immune cells as mechanisms contributing to altered mitral valve biomechanics post–myocardial infarction.

M-creatine kinase gene expression in mechanically overloaded skeletal muscle of transgenic mice

1995 ◽  
Vol 269 (3) ◽  
pp. C665-C674 ◽  
Author(s):  
R. W. Tsika ◽  
S. D. Hauschka ◽  
L. Gao
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Creatine Kinase ◽  
Kinase Gene ◽  
Mouse Muscle ◽  
Average Decrease ◽  
Mechanical Overload ◽  
Mouse Lines ◽  
Specific Mrna

The molecular pathways and regulatory molecules that underlie changes in gene transcription during mechanical overload of skeletal muscle remain obscure. To better understand this process, we have examined mouse muscle creatine kinase (MCK) gene expression in mechanically overloaded plantaris (OP) muscle of transgenic and nontransgenic mice. Northern blot analysis revealed that endogenous MCK-specific mRNA transcripts were decreased 150% in the OP muscles after 6 wk. To identify the MCK gene regions involved in the response to mechanical overload, three different mouse MCKCAT transgenes were studied by measuring chloramphenicol acetyltransferase (CAT assays) activity in OP and sham-operated (control plantaris) muscles. Mouse lines carrying (+enh206)117MCKCAT and -1256MCKCAT transgenes exhibited 30 and 40% lower CAT levels, whereas two mouse lines carrying -3300MCKCAT transgenes exhibited average decreases of 430%. Nearly identical results, including measurements of exogenous CAT mRNA, were obtained 2 days postoverload. Six weeks or 2 days of mechanical overload led to an average decrease in MM-CK isoprotein of 140%. These data provide evidence that mechanical overload induces changes in MCK gene expression that appear to be regulated by at least two portions of the MCK gene: the 206 base pair 5' enhancer and the -3,300 to -1,257 region.

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