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 Evaluation of Cardiovascular Experiment Animal

2021 ◽  
Vol 9 (12) ◽  
pp. 2305-2310
Author(s):  
Kirtane Ramesh Kirtane
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Time Course ◽  
Muscle Fibers ◽  
Early Mortality ◽  
Ground Substance ◽  
Coronary Artery Ligation ◽  
Time Intervals ◽  
In Vivo Models ◽  
Immunohistochemical Studies

Abstract: In vivo models of myocardial infarction induced by coronary artery ligation in rats usually suffer from high early mortality and a low rate of induction. This study investigated the time course initiation of chronic myocardial infarction in albino rats and the possibility of reducing early mortality rate due to myocardial infarction by modification of the surgical technique. CAL was carried out by passing the suture through the pericardial layer around the midway of the left anterior descending coronary artery including a small area of the myocardium to avoid mechanical damage to the heart geometry. In addition, the role of endothelin-1 in rat heart with congestive heart failure was critically assessed. Time course initiation experiments were designed by sacrificing the animals at different time intervals and by carrying out physiological, biochemical, histopathological, electron microscopical and immunohistochemical studies. Specific markers of myocardial injury, viz. cardiac troponin-T, high sensitivity C-reactive protein, lactate dehydrogenase and fibrinogen were measured at different time points. Serum marker enzymes and activities of lysosomal hydrolases were found to be elevated on the eighth day post-ligation. Histopathological studies demonstrated focal areas showing fibrovascular tissue containing fibroblasts, collagenous ground substance and numerous small capillaries replacing cardiac muscle fibers. Transmission electron micrographs exhibited mitochondrial changes of well-developed irreversible cardiac injury, viz. swelling, disorganization of cristae, appearance of mitochondrial amorphous matrix densities, and significant distortion of muscle fibers and distinct disruption of the intercalated discs. Immune blotting studies confirmed the presence of alpha 2-macroglobulin which supported the inflammatory response. The severity of the CMI was inferred by the measurement of the level of ET-1 in plasma and left ventricle which was significantly higher in the CMI rats than in the sham-operated rats. Immunohistochemical studies at different time intervals showed that there was a significant immunoexpression of ET-1 on the eighth day post-ligation. This study conclusively showed that ligation of left anterior descending artery minimised mortality and ET-1 was expressed during CMI.

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

scholarly journals Comparison of thrombus, gut, and oral microbiomes in Korean patients with ST-elevation myocardial infarction: a case–control study

2020 ◽  
Vol 52 (12) ◽  
pp. 2069-2079
Author(s):  
Ju-Seung Kwun ◽  
Si-Hyuck Kang ◽  
Hyo-Jung Lee ◽  
Han-Ki Park ◽  
Won-Jae Lee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Relative Abundance ◽  
Gut Microbiome ◽  
Case Control Study ◽  
Plaque Rupture ◽  
Case Control ◽  
Oral Microbiome ◽  
Healthy Controls ◽  
Control Study

AbstractST-segment elevation myocardial infarction (STEMI) is characterized by thrombotic coronary artery occlusions caused by atherosclerotic plaque rupture. The gut microbiome potentially contributes to the pathogenesis of coronary artery diseases. This study investigated the microbial diversity and composition of coronary thrombi in STEMI patients and the composition of the thrombus microbiome relative to that of the oral and gut microbiomes. A case–control study was performed with 22 STEMI patients and 20 age- and sex-matched healthy controls. Coronary thrombi were acquired from STEMI patients via manual thrombus aspiration during primary coronary intervention. Oral swab and stool samples were collected from both groups, and 16S rRNA sequencing and metagenomic microbiome analyses were performed. Microbial DNA was detected in 4 of 22 coronary thrombi. Proteobacteria (p) and Bacteroidetes (p) were the most abundant phyla. The oral and gut microbiomes significantly differed between patients and healthy controls. The patient group presented microbial dysbiosis, as follows: a higher relative abundance of Proteobacteria (p) and Enterobacteriaceae (f) in the gut microbiome and a lower abundance of Firmicutes (p) and Haemophilus (g) in the oral microbiome. Furthermore, 4 significantly abundant genera were observed in the coronary thrombus in the patients: Escherichia, 1.25%; Parabacteroides, 0.25%; Christensenella, 0.0%; and Bacteroides, 7.48%. The present results indicate that the relative abundance of the gut and oral microbiomes was correlated with that of the thrombus microbiome.

Effect of adrenocorticotropic hormone on UCP1 gene expression in brown adipocytes

2017 ◽  
Vol 28 (3) ◽  
Author(s):  
Hirendra M. Biswas
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Adrenocorticotropic Hormone ◽  
Northern Blot Analysis ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Brown Adipocytes ◽  
Camp Generation ◽  
Brown Adipose ◽  
Stimulation Of

AbstractBackground:Like other tissues, adrenocorticotropic hormone (ACTH) can produce its effect on brown adipose tissue (BAT). This study was taken to understand the direct effect of ACTH action on thermogenin gene expression and possible relation with α receptors and caffeine with this hormone.Methods:Brown fat precursor cells were isolated from interscapular BAT of young mice and grown in culture. The cells were exposed to norepinephrine (NE) and other agents. Total RNA was isolated after harvesting the cells, and northern blot analysis was performed. Hybridization was performed with nick translated cDNA probes. Filters were exposed to film, and results were evaluated by scanning. Cyclic adenosine monophosphate (cAMP) was measured by using Amersham assay kit.Results:ACTH stimulates thermogenin gene expression in brown adipocytes. Initiation and maximum stimulations are observed with 0.01 μM and 10 μM (about 45%) of ACTH, respectively, in comparison to 0.1 μM of NE. Maximum response of cAMP is also observed with 10 μM of ACTH (about 64%). Studies with cirazoline and ACTH show thatConclusions:ACTH stimulates thermogenin gene expression in cultured brown adipocytes. The complex interrelationship of ACTH with cirazoline indicates the possibility of relation between the activity of ACTH and α receptors in brown adipocytes. Further stimulation of cAMP generation and thermogenin gene expression is possible with ACTH in conjugation with caffeine and RO 20-1724.

Acute ST-segment elevation myocardial infarction in covid-19 patients: a single hospital experience

2021 ◽  
Vol 23 (1) ◽  
pp. 43-47
Author(s):  
Vakhtang I. Safaryan ◽  
◽  
Kirill A. Savostyanov ◽  
Kirill A. Savostyanov ◽  
Dmitry S. Sizgunov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Obstructive Coronary Artery Disease ◽  
Pain Syndrome ◽  
Time Intervals ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Artery Disease

The COVID-19 pandemic has dramatically changed the lives of people and the work of hospitals and the health system. The rapid spread of infection, high mortality and congestion in hospitals are of high concern. Due to insufficiently causes, the number of admissions of patients with acute coronary syndrome (ACS) has significantly decreased in many centers, while timely intervention significantly improves the prognosis of AMI patients with ST segment elevation. Aim. To assess the clinical characteristics of patients with ST-segment elevation AMI during the re-profiling of the center for patients with COVID-19. Materials and methods. In total, the center worked to receive patients with COVID-19 and ACS for one month, during which 8 AMI patients with ST segment elevation were hospitalized. SARS-CoV-2 was diagnosed on the basis of nasopharyngeal or oropharyngeal smear PCR, serum IgM and IgG, or lung CT, which were performed on the day of admission, regardless of the severity of the condition. Segment elevation AMI was diagnosed based on typical clinical presentations accompanied by ST-segment elevation or newly diagnosed LBBB. Stenosis was considered as an infarction-related lesion in the presence of angiographic signs of thrombotic occlusion or subocclusion. Obstructive coronary artery disease was defined as >50% stenosis based on visual assessment of angiography. Results. All patients had ST-segment elevation, 6 (75%) patients had typical pain syndrome, 2 (25%) patients had pain syndrome accompanied by shortness of breath. SARS-CoV-2 was detected by PCR in 4 (50%), in 2 (25%) – an increased titer of IgM and IgG. CT scan showed 7 (87.5%) changes characteristic of COVID-19. Severe (CT3) and moderately severe (CT2) lesions were found in 4 (50%) patients. All patients underwent coronary angiography, thrombolysis was not performed. All patients had obstructive coronary artery disease requiring revascularization. When compared with the same calendar interval of the previous 3 years, the decrease in hospitalization for AMI with ST elevation was 50% or more. However, when comparing pain-door and door-balloon time intervals, no significant differences were found (p=0.786 and p=0.300, respectively). Conclusion. All patients with suspected ST-segment elevation AMI had obstructive coronary artery disease requiring revascularization. There was a significant decrease in the number of patients with AMI with ST-segment elevation without changing the time intervals before hospitalization and intervention. Keywords: acute myocardial infarction, COVID-19, revascularization For citation: Safaryan VI, Savostyanov KA, Sizgunov DS, Sargsyan AZ, Birukov PA. Acute ST-segment elevation myocardial infarction in COVID-19 patients: a single hospital experience. Consilium Medicum. 2021; 23 (1): 43–47. DOI: 10.26442/20751753.2021.1.200574

scholarly journals Diagnosis of coronary heart diseases using gene expression profiling; stable coronary artery disease, cardiac ischemia with and without myocardial necrosis

2015 ◽  
Author(s):  
Nabila Kazmi ◽  
Tom Gaunt
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Unstable Angina ◽  
Stable Coronary Artery Disease ◽  
Myocardial Necrosis ◽  
Cardiac Ischemia ◽  
Myocardial Infraction ◽  
Artery Disease

AbstractCardiovascular disease including coronary artery disease and myocardial infarction is one of the leading causes of death in Europe, and is influenced by both environmental and genetic factors. With the advancements in genomic tools and technologies there is potential to predict and diagnose heart disease using molecular data from analysis of blood cells. We analyzed gene expression data from blood samples taken from normal people (n=21), non-significant coronary artery disease (n=93), patients with unstable angina (n=16), stable coronary artery disease (n=14) and myocardial infarction (MI; n=207). We used a feature selection approach to identify a set of gene expression variables which successfully differentiate different cardiovascular diseases. The initial features were discovered by fitting a linear model for each probe set across all arrays of normal individuals and patients with myocardial infarction. Three different feature optimisation algorithms were devised which identified two most discriminating sets of genes one using MI and normal controls (total genes=8) and another one using MI and unstable angina patients (total genes=17). The results proved the diagnostic robustness of the final feature sets in discriminating not only patients with myocardial infraction from healthy controls but also from patients with clinical symptoms of cardiac ischemia with myocardial necrosis and stable coronary artery disease despite the influence of batch effects and different microarray gene chips and platforms. selection approach to identify a set of gene expression variables which successfully differentiate different cardiovascular diseases. The initial features were discovered by fitting a linear model for each probe set across all arrays of normal individuals and patients with myocardial infarction. Three different feature optimisation algorithms were devised which identified two most discriminating sets of genes one using MI and normal controls (total genes=8) and another one using MI and unstable angina patients (total genes=17). The results proved the diagnostic robustness of the final feature sets in discriminating not only patients with myocardial infraction from healthy controls but also from patients with clinical symptoms of cardiac ischemia with myocardial necrosis and stable coronary artery disease despite the influence of batch effects and different microarray gene chips and platforms.

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