Effects of moderate exercise on lipopolysaccharide-induced inflammatory responses in rat's cardiac tissue

Porcine heart xenotransplantation is a potential treatment for patients with end-stage heart failure. To understand molecular mechanisms of graft rejection after heart transplantation, we transplanted a 31-day-old alpha-1,3-galactosyltransferase knockout (GTKO) porcine heart to a five-year-old cynomolgus monkey. Histological and transcriptome analyses were conducted on xenografted cardiac tissue at rejection (nine days after transplantation). The recipient monkey’s blood parameters were analyzed on days −7, −3, 1, 4, and 7. Validation was conducted by quantitative real-time PCR (qPCR) with selected genes. A non-transplanted GTKO porcine heart from an age-matched litter was used as a control. The recipient monkey showed systemic inflammatory responses, and the rejected cardiac graft indicated myocardial infarction and cardiac fibrosis. The transplanted heart exhibited a total of 3748 differentially expressed genes compared to the non-transplanted heart transcriptome, with 2443 upregulated and 1305 downregulated genes. Key biological pathways involved at the terminal stage of graft rejection were cardiomyopathies, extracellular interactions, and ion channel activities. The results of qPCR evaluation were in agreement with the transcriptome data. Transcriptome analysis of porcine cardiac tissue at graft rejection reveals dysregulation of the key molecules and signaling pathways, which play relevant roles on structural and functional integrities of the heart.

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Protective effects of paeonol on cardiovascular complications in diabetes mellitus involves modulation of PI3K /Akt-GSK-3β signalling, regulation of protease-activated receptor-1 expressions and down-regulation of inflammatory mediators

Bangladesh Journal of Pharmacology ◽

10.3329/bjp.v10i4.24334 ◽

2015 ◽

Vol 10 (4) ◽

pp. 903

Author(s):

Jun Li ◽

Ze-Qing Xu ◽

Ling Bao ◽

Zhi-Cao Li ◽

Jia-Xiang Qu

Keyword(s):

Diabetic Cardiomyopathy ◽

Inflammatory Mediators ◽

Cardiac Tissue ◽

Inflammatory Responses ◽

Glycogen Synthase ◽

Serum Levels ◽

Protective Effects ◽

Sprague Dawley ◽

Tnf Α ◽

Protease Activated Receptor 1

<p class="Abstract">The present study was taken as an effort to assess the effects of paeonol on diabetic cardiomyopathy. Diabetes was induced in separate groups of Sprague-Dawley rats using streptozotocin. Treatment group animals received paeonol (50, 100 or 200 mg/kg body weight/day; orally) 5 weeks after streptozotocin induction for 6 weeks. Paeonol strikingly reduced myocardial apoptosis and improved cardiac function and myocardial architecture. Serum levels of glucose, reactive oxygen species and inflammatory mediators (TNF-α, IL-6 and IL-1β) were significantly reduced with decreased accumulation of collagen in the cardiac tissue. Paeonol modulated p-Akt, glycogen synthase kinase-3β and glycogen synthase, while significantly down-regulated protease-activated receptor-1, caspase-3, TNF-α, NF-κB p65, and p-Iκ-Bα expressions. Paeonol effectively suppressed diabetic cardiomyopathy by improving myocardial function, regulating the inflammatory responses and Akt signalling.</p><p> </p>

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Cytopathology of Cardiac Tissue from Daunomycin-Treated Mice

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100066802 ◽

1971 ◽

Vol 29 ◽

pp. 550-551

Author(s):

Robert H. Liss ◽

Frances A. Cotton

Keyword(s):

Cardiac Tissue ◽

Cardiac Toxicity ◽

Drug Distribution ◽

Personal Communication ◽

Intravenous Dose ◽

Single Intravenous Dose ◽

Physiologic Saline ◽

Histopathologic Changes ◽

Distribution Studies ◽

Lung And Kidney

Daunomycin, an antibiotic used in the clinical management of acute leukemia, produces a delayed, lethal cardiac toxicity. The lethality is dose and schedule dependent; histopathologic changes induced by the drug have been described in heart, lung, and kidney from hamsters in both single and multiple dose studies. Mice given a single intravenous dose of daunomycin (10 mg/kg) die 6-7 days later. Drug distribution studies indicate that the rodents excrete most of a single dose of the drug as daunomycin and metabolite within 48 hours after dosage (M. A. Asbell, personal communication).Myocardium from the ventricles of 6 moribund BDF1 mice which had received a single intravenous dose of daunomycin (10 mg/kg), and from controls dosed with physiologic saline, was fixed in glutaraldehyde and prepared for electron microscopy.

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Iron storage sites in the myocardium as revealed by cytohistochemistry

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100104030 ◽

1988 ◽

Vol 46 ◽

pp. 394-395

Author(s):

M. Ashraf ◽

F. Thompson ◽

S. Miki ◽

P. Srivastava

Keyword(s):

Cardiac Tissue ◽

Coronary Perfusion ◽

Intracellular Iron ◽

Ether Anesthesia ◽

Intense Staining ◽

Iron Storage ◽

Thin Sections ◽

Rat Hearts ◽

Cacodylate Buffer ◽

Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

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Immunoelectron microscope detection of C-type natriuretic peptide in normal human atrial tissue

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100147776 ◽

1993 ◽

Vol 51 ◽

pp. 388-389

Author(s):

Chi-Ming Wei ◽

Margaret Hukee ◽

Christopher G.A. McGregor ◽

John C. Burnett

Keyword(s):

Amino Acid ◽

Natriuretic Peptide ◽

Vascular Tone ◽

Cardiac Tissue ◽

Ring Structure ◽

Terminal Amino Acid ◽

Amino Acid Peptide ◽

Normal Human ◽

Terminal Amino ◽

The Brain

C-type natriuretic peptide (CNP) is a newly identified peptide that is structurally related to atrial (ANP) and brain natriuretic peptide (BNP). CNP exists as a 22-amino acid peptide and like ANP and BNP has a 17-amino acid ring formed by a disulfide bond. Unlike these two previously identified cardiac peptides, CNP lacks the COOH-terminal amino acid extension from the ring structure. ANP, BNP and CNP decrease cardiac preload, but unlike ANP and BNP, CNP is not natriuretic. While ANP and BNP have been localized to the heart, recent investigations have failed to detect CNP mRNA in the myocardium although small concentrations of CNP are detectable in the porcine myocardium. While originally localized to the brain, recent investigations have localized CNP to endothelial cells consistent with a paracrine role for CNP in the control of vascular tone. While CNP has been detected in cardiac tissue by radioimmunoassay, no studies have demonstrated CNP localization in normal human heart by immunoelectron microscopy.

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Confocal imaging of calcium in intact ventricular muscle provides a new view of excitation-contraction coupling

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100166154 ◽

1996 ◽

Vol 54 ◽

pp. 738-739

Author(s):

W.G. Wier

Keyword(s):

Local Control ◽

Cardiac Tissue ◽

Cell Function ◽

Isolated Heart ◽

Cardiac Cells ◽

Confocal Imaging ◽

Ion Concentration ◽

Heart Cell ◽

Free Calcium ◽

Heart Cells

A fundamentally new understanding of cardiac excitation-contraction (E-C) coupling is being developed from recent experimental work using confocal microscopy of single isolated heart cells. In particular, the transient change in intracellular free calcium ion concentration ([Ca2+]i transient) that activates muscle contraction is now viewed as resulting from the spatial and temporal summation of small (∼ 8 μm3), subcellular, stereotyped ‘local [Ca2+]i-transients' or, as they have been called, ‘calcium sparks'. This new understanding may be called ‘local control of E-C coupling'. The relevance to normal heart cell function of ‘local control, theory and the recent confocal data on spontaneous Ca2+ ‘sparks', and on electrically evoked local [Ca2+]i-transients has been unknown however, because the previous studies were all conducted on slack, internally perfused, single, enzymatically dissociated cardiac cells, at room temperature, usually with Cs+ replacing K+, and often in the presence of Ca2-channel blockers. The present work was undertaken to establish whether or not the concepts derived from these studies are in fact relevant to normal cardiac tissue under physiological conditions, by attempting to record local [Ca2+]i-transients, sparks (and Ca2+ waves) in intact, multi-cellular cardiac tissue.

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