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Journal articles on the topic 'Myosin Myocardium'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Buttrick, P., C. Perla, A. Malhotra, D. Geenen, M. Lahorra, and J. Scheuer. "Effects of chronic dobutamine on cardiac mechanics and biochemistry after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (1991): H473—H479. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h473.

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After myocardial infarction in rats, muscle performance in the remaining hypertrophied myocardium deteriorates and is associated with a decrease in myosin adenosinetriphosphatase (ATPase) activity and a shift to the V3 myosin heavy-chain isoform. We have previously shown in another model of hypertrophy, secondary to renovascular hypertension, that chronic intermittent adrenergic stimulation with dobutamine (Db) can prevent this biochemical adaptation. The present study was undertaken to assess the effects of chronic Db treatment on cardiac mass, function, metabolism, and myosin biochemistry in

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2

Larue, Catherine, Charles Calzolari, Jocelyne Léger, Jean Léger, and Bernard Pau. "Immunoradiometric assay of myosin heavy chain fragments in plasma for investigation of myocardial infarction." Clinical Chemistry 37, no. 1 (1991): 78–82. http://dx.doi.org/10.1093/clinchem/37.1.78.

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Abstract Estimation of the extent and location of infarct is important for the prognosis and hence therapeutic strategy in patients with acute myocardial infarction (AMI). Because cardiac myosin is the major structural protein of the myocardium, and may thus reflect the extent of injured tissue, we established a new sensitive immunoradiometric assay, using a pair of monoclonal antibodies (Mabs) that specifically bind the myosin heavy chain fragments liberated from the myocyte into plasma after a heart attack. A first Mab is linked to a magnetic solid phase. A second Mab, radiolabeled with 125I

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3

Locher, Matthew R., Maria V. Razumova, Julian E. Stelzer, Holly S. Norman та Richard L. Moss. "Effects of low-level α-myosin heavy chain expression on contractile kinetics in porcine myocardium". American Journal of Physiology-Heart and Circulatory Physiology 300, № 3 (2011): H869—H878. http://dx.doi.org/10.1152/ajpheart.00452.2010.

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Myosin heavy chain (MHC) isoforms are principal determinants of work capacity in mammalian ventricular myocardium. The ventricles of large mammals including humans normally express ∼10% α-MHC on a predominantly β-MHC background, while in failing human ventricles α-MHC is virtually eliminated, suggesting that low-level α-MHC expression in normal myocardium can accelerate the kinetics of contraction and augment systolic function. To test this hypothesis in a model similar to human myocardium we determined composite rate constants of cross-bridge attachment ( fapp) and detachment ( gapp) in porci

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4

Suematsu, Nobuhiro, Shinji Satoh, Shintaro Kinugawa та ін. "α1-Adrenoceptor-Gq-RhoA signaling is upregulated to increase myofibrillar Ca2+ sensitivity in failing hearts". American Journal of Physiology-Heart and Circulatory Physiology 281, № 2 (2001): H637—H646. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h637.

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α1-Adrenergic stimulation, coupled to Gq, has been shown to promote heart failure. However, the role of α1-adrenergic signaling in the regulation of myocardial contractility in failing myocardium is still poorly understood. To investigate this, we observed 1) the effect of phenylephrine on myofibrillar Ca2+ sensitivity in α-toxin-skinned cardiomyocytes, and 2) protein expression of Gq, RhoA, and myosin light chain phosphorylation using tachypacing-induced canine failing hearts. Phenylephrine significantly increased myofibrillar Ca2+ sensitivity in failing but not in normal cardiomyocytes. Wher

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5

Khalina, Yana, Sergey Udaltsov, and Zoya A. Podlubnaya. "Ischemic myocardium: Behavior of myosin light chains." Journal of Molecular and Cellular Cardiology 34, no. 6 (2002): A84. http://dx.doi.org/10.1016/s0022-2828(02)91028-x.

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6

Gregorich, Zachery R., Jitandrakumar R. Patel, Wenxuan Cai, et al. "Deletion of Enigma Homologue from the Z-disc slows tension development kinetics in mouse myocardium." Journal of General Physiology 151, no. 5 (2019): 670–79. http://dx.doi.org/10.1085/jgp.201812214.

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Enigma Homologue (ENH) is a component of the Z-disc, a structure that anchors actin filaments in the contractile unit of muscle, the sarcomere. Cardiac-specific ablation of ENH protein expression causes contractile dysfunction that ultimately culminates in dilated cardiomyopathy. However, whether ENH is involved in the regulation of myocardial contractility is unknown. To determine if ENH is required for the mechanical activity of cardiac muscle, we analyze muscle mechanics of isolated trabeculae from the hearts of ENH+/+ and ENH−/− mice. We detected no differences in steady-state mechanical p

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7

Toepfer, Christopher N., Markus B. Sikkel, Valentina Caorsi, et al. "A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 2 (2016): H465—H475. http://dx.doi.org/10.1152/ajpheart.00899.2015.

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Myocardial remodeling in response to chronic myocardial infarction (CMI) progresses through two phases, hypertrophic “compensation” and congestive “decompensation.” Nothing is known about the ability of uninfarcted myocardium to produce force, velocity, and power during these clinical phases, even though adaptation in these regions likely drives progression of compensation. We hypothesized that enhanced cross-bridge-level contractility underlies mechanical compensation and is controlled in part by changes in the phosphorylation states of myosin regulatory proteins. We induced CMI in rats by le

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8

Patel, Jitandrakumar R., Daniel P. Fitzsimons, Scott H. Buck, Mariappan Muthuchamy, David F. Wieczorek та Richard L. Moss. "PKA accelerates rate of force development in murine skinned myocardium expressing α- or β-tropomyosin". American Journal of Physiology-Heart and Circulatory Physiology 280, № 6 (2001): H2732—H2739. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2732.

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In myocardium, protein kinase A (PKA) is known to phosphorylate troponin I (TnI) and myosin-binding protein-C (MyBP-C). Here, we used skinned myocardial preparations from nontransgenic (NTG) mouse hearts expressing 100% α-tropomyosin (α-Tm) to examine the effects of phosphorylated TnI and MyBP-C on Ca2+ sensitivity of force and the rate constant of force redevelopment ( k tr). Experiments were also done using transgenic (TG) myocardium expressing ∼60% β-Tm to test the idea that the α-Tm isoform is required to observe the mechanical effects of PKA phosphorylation. Compared with NTG myocardium,

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9

Ma, Weikang, Marcus Henze, Robert L. Anderson, et al. "The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium." Circulation Research 129, no. 6 (2021): 617–30. http://dx.doi.org/10.1161/circresaha.120.318647.

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Rationale: Myofilament length-dependent activation (LDA) is the key underlying mechanism of cardiac heterometric autoregulation, commonly referred as the Frank-Starling Law of the heart. Although alterations in LDA are common in cardiomyopathic states, the precise structural and biochemical mechanisms underlying LDA remain unknown. Objective: Here, we examine the role of structural changes in the thick filament during diastole, in particular changes in the availability of myosin heads, in determining both calcium sensitivity and maximum contractile force during systole in permeabilized porcine

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10

Bing, O. H., N. L. Hague, C. L. Perreault, et al. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (1994): H1112—H1121. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h1112.

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To examine the mechanisms by which thyroid hormone modulates the inotropic state of rat myocardium, we studied the effects of thyroid state on isolated rat left ventricular papillary muscle function and intracellular calcium transients in the baseline state and in response to calcium and isoproterenol. Marked differences in contractile state of papillary muscles from hypothyroid and thyroid hormone-treated rats seen under baseline conditions (1.0 mM bath calcium, 30 degrees C, stimulation rate 12/min) do not appear to be due to differences in intracellular calcium concentration ([Ca2+]i) or to

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11

Bobyk, V. I., D. V. Ryabenko, O. V. Sergienko, et al. "Experimental model of autoimmune myosin-induced myocardium injury." Biopolymers and Cell 23, no. 2 (2007): 115–21. http://dx.doi.org/10.7124/bc.00075d.

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12

Chen, Peter P., Jitandrakumar R. Patel, Inna N. Rybakova, Jeffery W. Walker, and Richard L. Moss. "Protein kinase A–induced myofilament desensitization to Ca2+ as a result of phosphorylation of cardiac myosin–binding protein C." Journal of General Physiology 136, no. 6 (2010): 615–27. http://dx.doi.org/10.1085/jgp.201010448.

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In skinned myocardium, cyclic AMP–dependent protein kinase A (PKA)-catalyzed phosphorylation of cardiac myosin–binding protein C (cMyBP-C) and cardiac troponin I (cTnI) is associated with a reduction in the Ca2+ responsiveness of myofilaments and an acceleration in the kinetics of cross-bridge cycling, although the respective contribution of these two proteins remains controversial. To further examine the relative roles that cTnI and cMyBP-C phosphorylation play in altering myocardial function, we determined the Ca2+ sensitivity of force (pCa50) and the activation dependence of the rate of for

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13

Shimkunas, Rafael, Om Makwana, Kimberly Spaulding, et al. "Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 8 (2014): H1150—H1158. http://dx.doi.org/10.1152/ajpheart.00463.2014.

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After myocardial infarction, a poorly contracting nonischemic border zone forms adjacent to the infarct. The cause of border zone dysfunction is unclear. The goal of this study was to determine the myofilament mechanisms involved in postinfarction border zone dysfunction. Two weeks after anteroapical infarction of sheep hearts, we studied in vitro isometric and isotonic contractions of demembranated myocardium from the infarct border zone and a zone remote from the infarct. Maximal force development (Fmax) of the border zone myocardium was reduced by 31 ± 2% versus the remote zone myocardium (

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14

Klibanov, Alexander L., Ban An Khaw, Naseem Nossiff, et al. "Targeting of macromolecular carriers and liposomes by antibodies to myosin heavy chain." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 4 (1991): L60—L65. http://dx.doi.org/10.1152/ajplung.1991.261.4.l60.

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Macromolecular carriers and liposomes were covalently coupled to monoclonal antibodies against cardiac myosin heavy chain. Deferoxamine-modified polymers bound tightly with 67Ga and68 Ga radioisotopes. Ternary deferoxamine-polylysine antibody conjugates specifically targeted the radioisotopes to a myosin-coated microplate. Scatchard analysis revealed a high affinity of the conjugate for the target with a Kas of ≈108 M-1. Liposomes that contained immobilized antimyosin antibodies were targeted specifically to the myosin-coated plate. Additional coating of these liposomes with polyethylene glyco

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15

Klibanov, Alexander L., Ban An Khaw, Naseem Nossiff, et al. "Targeting of macromolecular carriers and liposomes by antibodies to myosin heavy chain." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (1991): 60–65. http://dx.doi.org/10.1152/ajpheart.1991.261.4.60.

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Macromolecular carriers and liposomes were covalently coupled to monoclonal antibodies against cardiac myosin heavy chain. Deferoxamine-modified polymers bound tightly with 67Ga and 68Ga radioisotopes. Ternary deferoxamine-polylysine antibody conjugates specifically targeted the radioisotopes to a myosin-coated microplate. Scatchard analysis revealed a high affinity of the conjugate for the target with a Kas of ≈108 M-1. Liposomes that contained immobilized antimyosin antibodies were targeted specifically to the myosin-coated plate. Additional coating of these liposomes with polyethylene glyco

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16

SCHIAFFINO, S., L. GORZA, S. SARTORE, and L. SAGGIN. "Cardiac myosins: Distribution of myosin heavy chain isoforms in ordinary myocardium and conduction tissue." Journal of Molecular and Cellular Cardiology 17 (1985): 33. http://dx.doi.org/10.1016/s0022-2828(85)80243-1.

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17

Nishikawa, T., S. Ishiyama, K. Takeda, et al. "Programmed Cell Death (Apoptosis) in the Myocardium with Acute Myocarditis." Microscopy and Microanalysis 3, S2 (1997): 63–64. http://dx.doi.org/10.1017/s1431927600007200.

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Acute myocarditis is a potentially lethal disease. However, the precise mechanism of myocardial damage in myocarditis is still unknown, although its pathogenesis seems to be involved in the result of natural killer cells, cytotoxic T cells and autoantibodies. Recently, it has been reported that programmed death of cardiac myocytes can be induced by several pathological conditions including infarction and end-stage cardiac failure. However, little is known about the myocardial cell death in myocarditis. In this study, we investigated whether myocardial cell death via apoptosis occurs in the hea

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18

Hornby, L., N. Hamilton, D. Marshall, T. A. Salerno, M. H. Laughlin, and C. D. Ianuzzo. "Role of cardiac work in regulating myocardial biochemical characteristics." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (1990): H1482—H1490. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1482.

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The purpose of this study was to determine the extent to which functional demand regulates the biochemical character and enzyme capacities of the rat myocardium. Hearts from donor rats were heterotopically transplanted onto the abdominal aorta and inferior vena cava of isogenic recipients. The procedure results in a perfused but nonpumping heart that has a reduced heart rate (HR) and performs essentially no stroke work (SW). After 30 days, metabolic enzyme activities (phosphorylase, 6-phosphofructokinase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase) were significantly lower (40-60%)

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19

Rao, Vijay S., Laura R. La Bonte, Yaqin Xu, Zequan Yang, Brent A. French, and William H. Guilford. "Alterations to myofibrillar protein function in nonischemic regions of the heart early after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (2007): H654—H659. http://dx.doi.org/10.1152/ajpheart.01314.2006.

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Remote-zone left ventricular dysfunction (LVD) contributes to global reductions in contractile function after localized myocardial infarction (MI). However, the molecular mechanisms underlying this form of LVD are not clear. This study tested the hypothesis that myofibrillar protein function is directly affected in remote-zone LVD early after MI. Cardiac myosin and native thin filaments were purified from mouse myocardium taken from both the nonnecrotic zone adjacent to and the nonischemic zone remote from an infarct induced by 1 h of coronary occlusion followed by 24 h of reperfusion. Thin fi

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20

SILVER, P., L. BUJA, and J. STULL. "Frequency-dependent myosin light chain phosphorylation in isolated myocardium." Journal of Molecular and Cellular Cardiology 18, no. 1 (1986): 31–37. http://dx.doi.org/10.1016/s0022-2828(86)80980-4.

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21

Tanner, Bertrand C. W., Michael J. Previs, Yuan Wang, Jeffrey Robbins та Bradley M. Palmer. "Cardiac myosin binding protein-C phosphorylation accelerates β-cardiac myosin detachment rate in mouse myocardium". American Journal of Physiology-Heart and Circulatory Physiology 320, № 5 (2021): H1822—H1835. http://dx.doi.org/10.1152/ajpheart.00673.2020.

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Length perturbation analysis was used to demonstrate that β-cardiac myosin characteristic rates of detachment and recruitment in the intact myofilament lattice are accelerated by Pi, phosphorylation of cMyBP-C, and the absence of cMyBP-C. The results suggest that cMyBP-C normally slows myosin detachment, including Pi-dependent detachment, and that this inhibition is released with phosphorylation or absence of cMyBP-C.

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22

Stelzer, Julian E., Jitandrakumar R. Patel, and Richard L. Moss. "Acceleration of Stretch Activation in Murine Myocardium due to Phosphorylation of Myosin Regulatory Light Chain." Journal of General Physiology 128, no. 3 (2006): 261–72. http://dx.doi.org/10.1085/jgp.200609547.

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The regulatory light chains (RLCs) of vertebrate muscle myosins bind to the neck region of the heavy chain domain and are thought to play important structural roles in force transmission between the cross-bridge head and thick filament backbone. In vertebrate striated muscles, the RLCs are reversibly phosphorylated by a specific myosin light chain kinase (MLCK), and while phosphorylation has been shown to accelerate the kinetics of force development in skeletal muscle, the effects of RLC phosphorylation in cardiac muscle are not well understood. Here, we assessed the effects of RLC phosphoryla

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Pulcastro, Hannah C., Peter O. Awinda, Jason J. Breithaupt, and Bertrand C. W. Tanner. "Effects of myosin light chain phosphorylation on length-dependent myosin kinetics in skinned rat myocardium." Archives of Biochemistry and Biophysics 601 (July 2016): 56–68. http://dx.doi.org/10.1016/j.abb.2015.12.014.

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24

Sarin, Vandana, Mariappan Muthuchamy, and Cristine L. Heaps. "Ca2+ sensitization of cardiac myofilament proteins contributes to exercise training-enhanced myocardial function in a porcine model of chronic occlusion." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (2011): H1579—H1587. http://dx.doi.org/10.1152/ajpheart.00294.2011.

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Exercise training has been shown to improve cardiac dysfunction in both patients and animal models of coronary artery disease; however, the underlying cellular and molecular mechanisms have not been completely understood. We hypothesized that exercise training would improve force generation in the myocardium distal to chronic coronary artery occlusion via altered intracellular Ca2+ concentration ([Ca2+]i) cycling and/or Ca2+ sensitization of myofilaments. Ameroid occluders were surgically placed around the proximal left circumflex coronary artery of adult female Yucatan pigs. Twenty-two weeks

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Wehman, Brody, Sudhish Sharma, Nicholas Pietris, et al. "Mesenchymal stem cells preserve neonatal right ventricular function in a porcine model of pressure overload." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (2016): H1816—H1826. http://dx.doi.org/10.1152/ajpheart.00955.2015.

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Limited therapies exist for patients with congenital heart disease (CHD) who develop right ventricular (RV) dysfunction. Bone marrow-derived mesenchymal stem cells (MSCs) have not been evaluated in a preclinical model of pressure overload, which simulates the pathophysiology relevant to many forms of CHD. A neonatal swine model of RV pressure overload was utilized to test the hypothesis that MSCs preserve RV function and attenuate ventricular remodeling. Immunosuppressed Yorkshire swine underwent pulmonary artery banding to induce RV dysfunction. After 30 min, human MSCs (1 million cells, n =

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Li, King-Lun, Mei Methawasin, Bertrand C. W. Tanner, Henk L. Granzier, R. John Solaro, and Wen-Ji Dong. "Sarcomere length–dependent effects on Ca2+-troponin regulation in myocardium expressing compliant titin." Journal of General Physiology 151, no. 1 (2018): 30–41. http://dx.doi.org/10.1085/jgp.201812218.

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Cardiac performance is tightly regulated at the cardiomyocyte level by sarcomere length, such that increases in sarcomere length lead to sharply enhanced force generation at the same Ca2+ concentration. Length-dependent activation of myofilaments involves dynamic and complex interactions between a multitude of thick- and thin-filament components. Among these components, troponin, myosin, and the giant protein titin are likely to be key players, but the mechanism by which these proteins are functionally linked has been elusive. Here, we investigate this link in the mouse myocardium using in sit

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Liu, Haidun, Mary Henein, Maria Anillo, and John F. Dawson. "Cardiac actin changes in the actomyosin interface have different effects on myosin duty ratio." Biochemistry and Cell Biology 96, no. 1 (2018): 26–31. http://dx.doi.org/10.1139/bcb-2017-0136.

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Hypertrophic cardiomyopathy (HCM) is an inherited cardiovascular disease (CD) that commonly causes an increased size of cardiomyocytes in the left ventricle. The proteins myosin and actin interact in the myocardium to produce contraction through the actomyosin ATPase cycle. The duty ratio (r) of myosin is the proportion of the actomyosin ATPase cycle that myosin is bound to actin and does work. A common hypothesis is that HCM mutations increase contraction in cardiac sarcomeres; however, the available data are not clear on this connection. Based on previous work with human α-cardiac actin (ACT

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Laughlin, M. H., C. C. Hale, L. Novela, D. Gute, N. Hamilton, and C. D. Ianuzzo. "Biochemical characterization of exercise-trained porcine myocardium." Journal of Applied Physiology 71, no. 1 (1991): 229–35. http://dx.doi.org/10.1152/jappl.1991.71.1.229.

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The purpose of this study was to determine whether cardiac biochemical adaptations are induced by chronic exercise training (ET) of miniature swine. Female Yucatan miniature swine were trained on a treadmill or were cage confined (C) for 16–22 wk. After training, the ET pigs had increased exercise tolerance, lower heart rates during exercise at submaximal intensities, moderate cardiac hypertrophy, increased coronary blood flow capacity, and increased oxidative capacity of skeletal muscle. Myosin from both the C and ET hearts was 100% of the V3 isozyme, and there were no differences between the

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Parker, Thomas G., та James N. Tsoporis. "Induction of S100β in Myocardium: An Intrinsic Inhibitor of Cardiac Hypertrophy". Canadian Journal of Applied Physiology 23, № 4 (1998): 377–89. http://dx.doi.org/10.1139/h98-022.

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Cardiac hypertrophy induced by pressure overload and following myocardial infarction entails regulation of myocardial gene expression, recapitulating an embryonic phenotype, including activation of fetal β-myosin heavy chain and skeletal α-actin. Progressive hypertrophy and alterations in gene expression may contribute to myocardial failure. Although signaling pathways that contribute to hypertrophy development have been identified, intrinsic cardiac regulators that limit hypertrophic response have not been determined. The β subunit of S100 protein is induced in the myocardium of human subject

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Ait-Mou, Younss, Karen Hsu, Gerrie P. Farman, et al. "Titin strain contributes to the Frank–Starling law of the heart by structural rearrangements of both thin- and thick-filament proteins." Proceedings of the National Academy of Sciences 113, no. 8 (2016): 2306–11. http://dx.doi.org/10.1073/pnas.1516732113.

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The Frank–Starling mechanism of the heart is due, in part, to modulation of myofilament Ca2+ sensitivity by sarcomere length (SL) [length-dependent activation (LDA)]. The molecular mechanism(s) that underlie LDA are unknown. Recent evidence has implicated the giant protein titin in this cellular process, possibly by positioning the myosin head closer to actin. To clarify the role of titin strain in LDA, we isolated myocardium from either WT or homozygous mutant (HM) rats that express a giant splice isoform of titin, and subjected the muscles to stretch from 2.0 to 2.4 μm of SL. Upon stretch, H

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Bottinelli, R., M. Canepari, V. Cappelli, and C. Reggiani. "Maximum speed of shortening and ATPase activity in atrial and ventricular myocardia of hyperthyroid rats." American Journal of Physiology-Cell Physiology 269, no. 3 (1995): C785—C790. http://dx.doi.org/10.1152/ajpcell.1995.269.3.c785.

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The kinetic properties of the myofibrillar system of atrial and ventricular myocardia of hyperthyroid rats were analyzed by determining ATPase activity and maximum shortening velocity. Hyperthyroidism was induced by daily subcutaneous injections of triiodothyronine (0.2 mg/kg body wt) for 2 wk. The treatment induced a marked atrial and ventricular hypertrophy and, in ventricular myocardium, an isomyosin shift toward a homogeneous V1 composition. Skinned trabeculae and purified myofibrils were prepared from atrial and ventricular myocardia. Enzymatic assays on the myofibrils showed that both Ca

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Wang, Guan-Ying, Diana T. McCloskey, Sally Turcato, Philip M. Swigart, Paul C. Simpson та Anthony J. Baker. "Contrasting inotropic responses to α1-adrenergic receptor stimulation in left versus right ventricular myocardium". American Journal of Physiology-Heart and Circulatory Physiology 291, № 4 (2006): H2013—H2017. http://dx.doi.org/10.1152/ajpheart.00167.2006.

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The left ventricle (LV) and right ventricle (RV) have differing hemodynamics and embryological origins, but it is unclear whether they are regulated differently. In particular, no previous studies have directly compared the LV versus RV myocardial inotropic responses to α1-adrenergic receptor (α1-AR) stimulation. We compared α1-AR inotropy of cardiac trabeculae from the LV versus RV of adult mouse hearts. As previously reported, for mouse RV trabeculae, α1-AR stimulation with phenylephrine (PE) caused a triphasic contractile response with overall negative inotropy. In marked contrast, LV trabe

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Mozaffari, Mahmood S., Glenn L. Wilson, and Stephen W. Schaffer. "Effect of chronic sulfonylurea treatment on the myocardium of insulin-dependent diabetic rats." Canadian Journal of Physiology and Pharmacology 66, no. 12 (1988): 1481–86. http://dx.doi.org/10.1139/y88-242.

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Adult rats treated with high doses of streptozocin became progressively more hyperglycemic during the first month of the diabetic condition. Treatment of these rats with the sulfonylurea glyburide halted, and in some cases, reversed this process in a high percentage of the diabetics. Associated with the glyburide-mediated improvement in fasting blood glucose levels was an increase in myocardial glucose utilization and lactate production. The stimulation of myocardial glucose utilization by insulin was greater in glyburide-treated hearts, indicating that the hyperglycemic agent increased insuli

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Stepanova, O. V., A. V. Chadin, A. A. Raevskaya, D. A. Blejyants, R. M. Muratov, and V. P. Shirinsky. "Myosin-activating protein kinases in human myocardium: Localization and content." Biophysics 53, no. 5 (2008): 366–70. http://dx.doi.org/10.1134/s0006350908050084.

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35

Syrový, I. "Expression of myosin in atrial areas of the bovine myocardium." Comparative Biochemistry and Physiology Part A: Physiology 92, no. 3 (1989): 441–43. http://dx.doi.org/10.1016/0300-9629(89)90589-6.

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36

LYN, DEBORAH, XIAOWEI LIU, NICOLE A. BENNETT, and NERIMIAH L. EMMETT. "Gene expression profile in mouse myocardium after ischemia." Physiological Genomics 2, no. 3 (2000): 93–100. http://dx.doi.org/10.1152/physiolgenomics.2000.2.3.93.

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Lyn, Deborah, Xiaowei Liu, Nicole A. Bennett, and Nerimiah L. Emmett. Gene expression profile in mouse myocardium after ischemia. Physiol Genomics 2: 93–100, 2000.—This study was designed to elaborate a molecular profile of expressed genes during ischemic injury to the mouse heart after surgical constriction of the left coronary artery without reperfusion. A mouse cDNA array containing 588 known genes was used to compare gene expression in heart RNA after 24-h ischemia with control tissue. Alterations in gene expression on the array were supported by relative reverse transcription-polymerase c

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Ianuzzo, C. D., S. Brotherton, P. O'Brien, T. Salerno, and M. H. Laughlin. "Myocardial biochemical and hemodynamic adaptations to chronic tachycardia." Journal of Applied Physiology 70, no. 2 (1991): 907–13. http://dx.doi.org/10.1152/jappl.1991.70.2.907.

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The purpose was to determine the biochemical and hemodynamic adaptations of the myocardium to chronic tachycardia. Cardiac pacemakers were implanted in Yorkshire pigs and set at a rate of 180 beats/min for a period of 35-42 days. Animals were then anesthetized with pentobarbital sodium. Myocardial blood flow and hemodynamics were determined at three different heart rates (i.e., 120, 180, and 220 beats/min). Tissue samples were then taken for microsphere and biochemical analyses. Chronically paced hearts maintained better cardiac function and had consistently higher left ventricular blood flow

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Dale, J. B., and E. H. Beachey. "Sequence of myosin-crossreactive epitopes of streptococcal M protein." Journal of Experimental Medicine 164, no. 5 (1986): 1785–90. http://dx.doi.org/10.1084/jem.164.5.1785.

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Group A streptococcal M proteins contain epitopes that crossreact with sarcolemmal membrane proteins of human myocardium and myosin. In the present study, synthetic peptide copies spanning the entire 197-residue pepsin extracted fragment of type 5 M protein were used to localize the myosin-crossreactive epitopes of the molecule. Peptide 84-116 inhibited by 75% the binding of myosin-crossreactive antibodies evoked by pep M5, as determined by ELISA. Immunoblot inhibition studies confirmed that peptide 84-116 almost totally inhibited the binding of pep M5 antibodies to the heavy chain of human ca

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Palmer, Bradley M., David E. Fishbaugher, Joachim P. Schmitt, et al. "Differential cross-bridge kinetics of FHC myosin mutations R403Q and R453C in heterozygous mouse myocardium." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (2004): H91—H99. http://dx.doi.org/10.1152/ajpheart.01015.2003.

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The kinetic effects of the cardiac myosin point mutations R403Q and R453C, which underlie lethal forms of familial hypertrophic cardiomyopathy (FHC), were assessed using isolated myosin and skinned strips taken from heterozygous (R403Q/+ and R453C/+) male mouse hearts. Compared with wild-type (WT) mice, actin-activated ATPase was increased by 38% in R403Q/+ and reduced by 45% in R453C/+, maximal velocity of regulated thin filament ( VRTF) in the in vitro motility assay was increased by 8% in R403Q/+ and was not different in R453C/+, myosin concentration at half-maximal VRTF was reduced by 30%

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Nassar, Rashid, Nadia N. Malouf, Lan Mao, et al. "cTnT1, a cardiac troponin T isoform, decreases myofilament tension and affects the left ventricular pressure waveform." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (2005): H1147—H1156. http://dx.doi.org/10.1152/ajpheart.00140.2004.

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Four isoforms of cardiac troponin T (cTnT), a protein essential for calcium-dependent myocardial force development, are expressed in the human; they differ in charge and length. Their expression is regulated developmentally and is affected by disease states. Human cTnT (hcTnT) isoform effects have been examined in reconstituted myofilaments. In this study, we evaluated the modulatory effects of overexpressing one cTnT isoform on in vitro and in vivo myocardial function. A hcTnT isoform, hcTnT1, expressed during development and in heart disease but not in the normal adult heart, was expressed i

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Palaniyandi, Suresh S., Yusuke Nagai, Kenichi Watanabe, et al. "Chymase Inhibition Reduces the Progression to Heart Failure After Autoimmune Myocarditis in Rats." Experimental Biology and Medicine 232, no. 9 (2007): 1213–21. http://dx.doi.org/10.3181/0703-rm-85.

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Chymase has been known as a local angiotensin II–generating enzyme in the cardiovascular system in dogs, monkeys, hamsters, and humans; however, recently it was reported that chymase also has various other functions. Therefore, we decided to examine whether the inhibition of chymase improves disease conditions associated with the pathophysiology of dilated cardiomyopathy in rats and its possible mechanism of action as rat chymase is unable to produce angiotensin II. We examined the effect of TY-51469, a novel chymase inhibitor (0.1 mg/kg/day [group CYI-0.1, n = 15] and 1 mg/kg/day [group CYI-1

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Colson, Brett A., Tanya Bekyarova, Daniel P. Fitzsimons, Thomas C. Irving, and Richard L. Moss. "Radial displacement of myosin cross-bridges in mouse myocardium due to ablation of myosin binding protein-C." Journal of Molecular and Cellular Cardiology 42, no. 6 (2007): S118. http://dx.doi.org/10.1016/j.yjmcc.2007.03.272.

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Colson, Brett A., Tanya Bekyarova, Daniel P. Fitzsimons, Thomas C. Irving, and Richard L. Moss. "Radial Displacement of Myosin Cross-bridges in Mouse Myocardium due to Ablation of Myosin Binding Protein-C." Journal of Molecular Biology 367, no. 1 (2007): 36–41. http://dx.doi.org/10.1016/j.jmb.2006.12.063.

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Gresham, Kenneth S., Ranganath Mamidi, Jiayang Li, Hyerin Kwak, and Julian E. Stelzer. "Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output." Journal of Applied Physiology 122, no. 3 (2017): 520–30. http://dx.doi.org/10.1152/japplphysiol.00306.2016.

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Molecular adaptations to chronic neurohormonal stress, including sarcomeric protein cleavage and phosphorylation, provide a mechanism to increase ventricular contractility and enhance cardiac output, yet the link between sarcomeric protein modifications and changes in myocardial function remains unclear. To examine the effects of neurohormonal stress on posttranslational modifications of sarcomeric proteins, mice were administered combined α- and β-adrenergic receptor agonists (isoproterenol and phenylephrine, IPE) for 14 days using implantable osmotic pumps. In addition to significant cardiac

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Vornanen, M. "Seasonal and temperature-induced changes in myosin heavy chain composition of crucian carp hearts." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 6 (1994): R1567—R1573. http://dx.doi.org/10.1152/ajpregu.1994.267.6.r1567.

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Myosin heavy chain isoforms of the ventricular myocardium from crucian carp (Carassius carassius L.) hearts were analyzed in different times of the year by gradient sodium dodecyl sulfate-polyacrylamide gel electrophoresis [K. A. Esser, M. O. Boluyt, and T. P. White, Am. J. Physiol. 255 (Heart Circ. Physiol. 24): H659-H663, 1988]. In winter only one myosin heavy chain type was present, but in summer about one-half of the winter myosin was replaced by more slowly moving summer myosin. The occurrence of summer myosin correlated with seasonal changes in water temperature of the pond, where the fi

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Min, Jiang-Yong, Yinke Yang, Kimber L. Converso, et al. "Transplantation of embryonic stem cells improves cardiac function in postinfarcted rats." Journal of Applied Physiology 92, no. 1 (2002): 288–96. http://dx.doi.org/10.1152/jappl.2002.92.1.288.

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Massive loss of cardiac myocytes after myocardial infarction (MI) is a common cause of heart failure. The present study was designed to investigate the improvement of cardiac function in MI rats after embryonic stem (ES) cell transplantation. MI in rats was induced by ligation of the left anterior descending coronary artery. Cultured ES cells used for cell transplantation were transfected with the marker green fluorescent protein (GFP). Animals in the treated group received intramyocardial injection of ES cells in injured myocardium. Compared with the MI control group injected with an equivale

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Stelzer, Julian E., Jitandrakumar R. Patel, M. Charlotte Olsson, Daniel P. Fitzsimons, Leslie A. Leinwand, and Richard L. Moss. "Expression of cardiac troponin T with COOH-terminal truncation accelerates cross-bridge interaction kinetics in mouse myocardium." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 4 (2004): H1756—H1761. http://dx.doi.org/10.1152/ajpheart.00172.2004.

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Transgenic mice expressing an allele of cardiac troponin T (cTnT) with a COOH-terminal truncation (cTnTtrunc) exhibit severe diastolic and mild systolic dysfunction. We tested the hypothesis that contractile dysfunction in myocardium expressing low levels of cTnTtrunc (i.e., <5%) is due to slowed cross-bridge kinetics and reduced thin filament activation as a consequence of reduced cross-bridge binding. We measured the Ca2+ sensitivity of force development [pCa for half-maximal tension generation (pCa50)] and the rate constant of force redevelopment ( ktr) in cTnTtrunc and wild-type (WT) sk

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YOSHIDA, Ken-ichi, Tohru HANAFUSA, Ryoji MATOBA, and Choei WAKASUGI. "Proteolysis of myosin and troponin in human myocardium of elderly subjects." Japanese Heart Journal 31, no. 5 (1990): 683–91. http://dx.doi.org/10.1536/ihj.31.683.

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Turcani, Marian, Dirk Thormaehlen, and Heinz Rupp. "Tedisamil attenuates foetal transformation of myosin in the hypertrophied rat myocardium." British Journal of Pharmacology 143, no. 5 (2004): 561–72. http://dx.doi.org/10.1038/sj.bjp.0705992.

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Li Shaowei and Yang Tongshu. "Analysis of myosin light chains in myocardium from Keshan disease patients." Journal of Molecular and Cellular Cardiology 24 (May 1992): 222. http://dx.doi.org/10.1016/0022-2828(92)90690-2.

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