Alterations in Cardiac Tissue of a Natural Obese Rat Model: Implications for Obesity-Associated Cardiomyopathy

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC(4) concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.

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Effects in renal and cardiac tissue from CKD rat model: antioxidant evaluation of treatment with the selective endothelin‐receptor antagonist atrasentan and the combination of atrasentan with the vitamin D receptor activator (paricalcitol), and the angiot (404.4)

The FASEB Journal ◽

10.1096/fasebj.28.1_supplement.404.4 ◽

2014 ◽

Vol 28 (S1) ◽

Author(s):

Kevin Muñoz ◽

Eduardo Slatopolsky ◽

Sarah Zhang ◽

Jane Finch ◽

Helen Liapis ◽

...

Keyword(s):

Vitamin D ◽

Receptor Antagonist ◽

Vitamin D Receptor ◽

Rat Model ◽

Cardiac Tissue ◽

Endothelin Receptor Antagonist ◽

Endothelin Receptor ◽

Receptor Activator ◽

Antioxidant Evaluation

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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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