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6. Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice

Author

McConnell, Bradley K., Jones, Karen A., Fatkin, Diane, Arroyo, Luis H., Lee, Richard T., Aristizabal, Orlando, Turnbull, Daniel H., Georgakopoulos, Dimitrios, Kass, David, Bond, Meredith, Niimura, Hideshi, Schoen, Frederick J., Conner, David, Fischman, Donald H., Seidman, Christine E., and Seidman, J. G.

Published
1999

10. Disruption of Protein Kinase A Interaction with A-kinase-anchoring Proteins in the Heart in Vivo: EFFECTS ON CARDIAC CONTRACTILITY, PROTEIN KINASE A PHOSPHORYLATION, AND TROPONIN I PROTEOLYSIS*

Author

McConnell, Bradley K., Popovic, Zoran, Mal, Niladri, Lee, Kwangdeok, Bautista, James, Forudi, Farhad, Schwartzman, Raul, Jin, J.-P., Penn, Marc, and Bond, Meredith

Subjects
Male, Cardiotonic Agents, Myocardium, Mechanisms of Signal Transduction, Calcium-Binding Proteins, Troponin I, Isoproterenol, A Kinase Anchor Proteins, Gene Expression, Cyclic AMP-Dependent Protein Kinase Type II, Ryanodine Receptor Calcium Release Channel, Stroke Volume, macromolecular substances, musculoskeletal system, Myocardial Contraction, Adenoviridae, Rats, Mice, Transduction, Genetic, cardiovascular system, Animals, Phosphorylation, Peptides
Abstract

Protein kinase A (PKA)-dependent phosphorylation is regulated by targeting of PKA to its substrate as a result of binding of regulatory subunit, R, to A-kinase-anchoring proteins (AKAPs). We investigated the effects of disrupting PKA targeting to AKAPs in the heart by expressing the 24-amino acid regulatory subunit RII-binding peptide, Ht31, its inactive analog, Ht31P, or enhanced green fluorescent protein by adenoviral gene transfer into rat hearts in vivo. Ht31 expression resulted in loss of the striated staining pattern of type II PKA (RII), indicating loss of PKA from binding sites on endogenous AKAPs. In the absence of isoproterenol stimulation, Ht31-expressing hearts had decreased +dP/dtmax and -dP/dtmin but no change in left ventricular ejection fraction or stroke volume and decreased end diastolic pressure versus controls. This suggests that cardiac output is unchanged despite decreased +dP/dt and -dP/dt. There was also no difference in PKA phosphorylation of cardiac troponin I (cTnI), phospholamban, or ryanodine receptor (RyR2). Upon isoproterenol infusion, +dP/dtmax and -dP/dtmin did not differ between Ht31 hearts and controls. At higher doses of isoproterenol, left ventricular ejection fraction and stroke volume increased versus isoproterenol-stimulated controls. This occurred in the context of decreased PKA phosphorylation of cTnI, RyR2, and phospholamban versus controls. We previously showed that expression of N-terminal-cleaved cTnI (cTnI-ND) in transgenic mice improves cardiac function. Increased cTnI N-terminal truncation was also observed in Ht31-expressing hearts versus controls. Increased cTnI-ND may help compensate for reduced PKA phosphorylation as occurs in heart failure.

Published
2009

12. Measurement of Subcellular CA2+ Redistribution in Cardiac Muscle In Situ: Time Resolved Rapid Freezing and Electron Probe Microanalysis

Author

Bond, Meredith, Schluchter, Mark D., Keller, Eva, and Moravec, Christine S.

Subjects
mitochondria, cryosection, analysis of variance, calcium, Electron probe microanalysis, heart, papillary muscle, contractile force, junctional sarcoplasmic reticulum, Biology, time-resolved rapid freezing
Abstract

To directly assess the physiological roles of sarcoplasmic reticulum (SR) and miitochondria (MT), we have utilized energy dispersive electron probe microanalysis (EPMA) on ultrathin freeze-dried cryosections from isolated papillary muscles, rapidly frozen at precise time points of the contractile cycle. Using this approach, we can detect redistribution of subcellular Ca2+ during the cardiac contractile cycle. Changes in Ca2+ of less than 1.0 mmol/kg dry wt can be detected. By determining the variability of the Ca2+ measurements in preliminary experiments, we have also demonstrated that it is possible to optimize experimental design, i.e., to predict the number of animals per treatment group and the number of X-ray spectra per animal that are required in order to detect a specified Ca2+ difference. Quantitative EPMA of rapidly frozen contracting papillary muscle has also allowed us to correlate the Ca2+ content of SR and MT with the contractile state of the muscle. Our results show a decrease of 40% in the amount of Ca2+ stored in the junctional SR during a cardiac muscle twitch, thus providing direct evidence for a role of the SR as a primary site of Ca2+ release. In addition, we have demonstrated dissociation between MT Ca2+ uptake and activation of regulatory enzymes, such as pyruvate dehydrogenase, indicating that MT Ca2+ uptake is not required for activation of MT metabolism.

Published
1994

23. Decreased SLIM1 Expression and Increased Gelsolin Expression in Failing Human Hearts Measured by High-Density Oligonucleotide Arrays

Author

Yang, Jiacheng, primary, Moravec, Christine S., additional, Sussman, Mark A., additional, DiPaola, Nicholas R., additional, Fu, Dechen, additional, Hawthorn, Lesley, additional, Mitchell, Christina A., additional, Young, James B., additional, Francis, Gary S., additional, McCarthy, Patrick M., additional, and Bond, Meredith, additional

Published
2000
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33. The gene expression fingerprint of human heart failure.

Author

Fen-Lai Tan, Moravec, Christine S., Jianbo Li, Apperson-Hansen, Carolyn, McCarthy, Patrick M., Young, James B., and Bond, Meredith

Subjects
HEART failure, GENE expression, GENETICS
Abstract

Identifies a gene expression fingerprint for heart failure. Statistical method to establish comprehensive cutoff point for identification of differentially-expressed genes; Differentiation of etiologies of heart failure by gene expression fingerprint; Gene clusters that show coordinated up- or downregulation in human heart failure.

Published
2002
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37. Detection of 31P nuclear magnetic resonance signals in brain by in vivoand freeze-trapped assays

Author

Chance, Britton, Nakase, Yuzo, Bond, Meredith, Leigh, John S., and McDonald, George

Abstract

The 31P NMR spectrum of energy-related metabolites under strictly aerobic conditions in rapidly respiring tissues under physiological conditions has been approached by the study of the 31P NMR signals in vivoand in freeze-trapped organs. Freezing the head of the anesthetized animal by liquid N2, excision of the brain tissue (white and gray matter) at -196°, and transfer to the NMR tube occurs without alteration of the metabolite concentrations. The sample is warmed to the region -15° to -10°, at which temperatures there is sufficient mobility for recording 31P NMR at concentrations characteristic of brain tissues (∼5 mM) with an adequate signal to noise ratio in 10 min but insufficient mobility for significant enzymatic activity. A ∼0.4-sec acquisition time is adequate for nuclear relaxation and a 10-min scan gives an adequate signal to noise ratio. Metabolism of creatine phosphate, Pi, and sugar phosphates occurs by 1 hr at -10° and 2 hr at -12°. Extrapolation of the approximately zero order kinetics of disappearance of creatine phosphate and appearance of Pisuggests that <10% of these two metabolites has been altered in the time of the first measurement.A comparison of the freeze-trapped state and the in vivometabolite pattern is afforded in preliminary experiments on the head of the living mouse (brain and skeletal tissue) in aerobic and anaerobic states. Longer relaxation times and mild hypoxia due to the restricted diameter of the NMR tube gives significantly lower creatine phosphate/ATP values for this condition. Both direct in vivoand freeze-trapped assays of energy-related metabolites afford excellent approaches to the detection of anoxia and to the evaluation of metabolic control in hypoxic conditions.

Published
1978
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42. Myopathic changes in murine skeletal muscle lacking synemin.

Author

García-Pelagio KP, Muriel J, O'Neill A, Desmond PF, Lovering RM, Lund L, Bond M, and Bloch RJ

Subjects
Animals, Biomechanical Phenomena, Costameres metabolism, Costameres pathology, Genotype, Intermediate Filament Proteins genetics, Male, Mice, Inbred C57BL, Mice, Knockout, Muscle Fatigue, Muscle Fibers, Fast-Twitch metabolism, Muscle Fibers, Fast-Twitch pathology, Muscle, Skeletal pathology, Muscle, Skeletal physiopathology, Muscular Diseases etiology, Muscular Diseases genetics, Muscular Diseases pathology, Muscular Diseases physiopathology, Phenotype, Running, Sarcolemma metabolism, Sarcolemma pathology, Intermediate Filament Proteins deficiency, Isometric Contraction, Muscle Strength, Muscle, Skeletal metabolism, Muscular Diseases metabolism
Abstract

Diseases of striated muscle linked to intermediate filament (IF) proteins are associated with defects in the organization of the contractile apparatus and its links to costameres, which connect the sarcomeres to the cell membrane. Here we study the role in skeletal muscle of synemin, a type IV IF protein, by examining mice null for synemin (synm-null). Synm-null mice have a mild skeletal muscle phenotype. Tibialis anterior (TA) muscles show a significant decrease in mean fiber diameter, a decrease in twitch and tetanic force, and an increase in susceptibility to injury caused by lengthening contractions. Organization of proteins associated with the contractile apparatus and costameres is not significantly altered in the synm-null. Elastimetry of the sarcolemma and associated contractile apparatus in extensor digitorum longus myofibers reveals a reduction in tension consistent with an increase in sarcolemmal deformability. Although fatigue after repeated isometric contractions is more marked in TA muscles of synm-null mice, the ability of the mice to run uphill on a treadmill is similar to controls. Our results suggest that synemin contributes to linkage between costameres and the contractile apparatus and that the absence of synemin results in decreased fiber size and increased sarcolemmal deformability and susceptibility to injury. Thus synemin plays a moderate but distinct role in fast twitch skeletal muscle., (Copyright © 2015 the American Physiological Society.)

Published
2015
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43. Association of chairs of physiology 2008 survey results.

Author

Cheeseman C and Bond M

Subjects
Data Collection, Faculty, Medical statistics & numerical data, Humans, North America, Physiology economics, Physiology trends, Schools, Medical economics, Schools, Medical trends, Physiology statistics & numerical data, Research Support as Topic statistics & numerical data, Salaries and Fringe Benefits statistics & numerical data, Schools, Medical statistics & numerical data
Published
2009

44. Acute cellular rejection following human heart transplantation is associated with increased expression of vitronectin receptor (integrin alphavbeta3).

Author

Yamani MH, Yang J, Masri CS, Ratliff NB, Bond M, Starling RC, McCarthy P, Plow E, and Young JB

Subjects
Acute Disease, Down-Regulation, Graft Rejection pathology, Heart Transplantation pathology, Humans, Immunohistochemistry, Middle Aged, Postoperative Period, Receptors, Vitronectin analysis, T-Lymphocytes immunology, Time Factors, Graft Rejection immunology, Heart Transplantation immunology, Receptors, Vitronectin metabolism
Abstract

The vitronectin receptor (integrin alphavbeta3), a cell-surface adhesion receptor, has been shown to play a significant role in endothelial cell migration, apoptosis, atherosclerosis, and T-lymphocyte activation. This study was undertaken to test the hypothesis that cardiac allograft rejection is associated with increased expression of alphavbeta3. We also determined whether fibronectin receptor (alpha5beta1) and tissue factor are up-regulated in the presence of acute cellular rejection. We evaluated endomyocardial biopsy specimens with histologic evidence of different degrees of acute cellular rejection (grade 0, n = 10; grade 1A, n = 10; grade 2, n = 10; grade 3A, n = 10). Biopsies were obtained 2-4weeks after cardiac transplantation. Immunoperoxidase staining was performed for alphavbeta3, tissue factor, and alpha5beta1, and protein levels were further determined by Western blot analysis. Specimens with grade 2 and grade 3A rejection showed positive staining of alphavbeta3 in lymphocytic aggregates and vascular endothelial cells. By immunoblotting, we identified significantly increased expression of alphavbeta3 in the presence of acute rejection, grade 2 (3-fold, p = 0.01) and grade 3A (3.6-fold, p = 0.005) compared to grade 0 and 1 A specimens. There was no evidence of increased expression of alpha5beta1 or tissue factor. Acute cellular rejection, a process characterized by T-lymphocyte activation and release of inflammatory cytokines, is associated with increased expression of alphavbeta3.

Published
2002
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