scholarly journals Thyroid hormone plus dual-specificity phosphatase-5 siRNA increases the number of cardiac muscle cells and improves left ventricular contractile function in chronic doxorubicin-injured hearts

Theranostics ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 4790-4808
Author(s):  
Lin Tan ◽  
Nikolay Bogush ◽  
Emmen Naqvi ◽  
John W. Calvert ◽  
Robert M. Graham ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Cardiac Muscle ◽  
Contractile Function ◽  
Muscle Cells ◽  
Left Ventricular ◽  
Cardiac Muscle Cells ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Short-Term Akt Activation in Cardiac Muscle Cells Improves Contractile Function in Failing Hearts

2012 ◽  
Vol 181 (6) ◽  
pp. 1969-1976 ◽  
Author(s):  
Ichiro Shiojima ◽  
Stephan Schiekofer ◽  
Jochen G. Schneider ◽  
Kurt Belisle ◽  
Kaori Sato ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Contractile Function ◽  
Muscle Cells ◽  
Short Term ◽  
Cardiac Muscle Cells ◽  
Akt Activation

Lipid Droplet Accumulation in Cardiac Muscle Cells of the Bat: Induction by Reserpine and Antagonism by Atropine

1975 ◽  
Vol 33 ◽  
pp. 534-535
Author(s):  
Martin Hagopian ◽  
Eladio A. Nunez ◽  
Michael D. Gershon
Keyword(s):  
Cardiac Muscle ◽  
Lipid Droplets ◽  
Single Injection ◽  
Sympathetic Innervation ◽  
Muscle Cells ◽  
Left Ventricular ◽  
High Dose ◽  
Cardiac Muscle Cells ◽  
Cardiac Sympathetic Innervation ◽  
Point Count

Reserpine has been shown to induce the accumulation of large numbers of lipid inclusions in cardiac muscle cells of the bat. This effect of reserpine is seen 24 hours after a single injection of 5 mg/kg of the drug. Since the action of reserpine can be antagonized by chemical sympathectomy with 6-hydroxydopamine and mimicked by norepinephrine, we have postulated the involvement of the cardiac sympathetic innervation in mediating reserpine's effect. In the present investigation we have examined the ability of atropine to prevent the accumulation of lipid droplets in cardiac muscle after a single injection of reserpine. Two dose schedules of atropine were tried. A high dose consisted of 3 injections, 9 mg/kg each, given intraperitoneally at 8 hour intervals beginning one hour prior to challenge with reserpine. A low dose consisted of 2 mg/kg given the same way. Left ventricular muscle was examined by electron microscopy and the relative cardiocyte volume occupied by lipid droplets was quantitated from electron micrographs by point count planimetry.

Effects of hypoxia on cardiac growth in neonatal rat

1976 ◽  
Vol 231 (5) ◽  
pp. 1445-1450 ◽  
Author(s):  
M Hollenberg ◽  
N Honbo ◽  
AJ Samorodin
Keyword(s):  
Body Weight ◽  
Left Ventricle ◽  
Cardiac Muscle ◽  
Neonatal Period ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Low Oxygen ◽  
Cardiac Muscle Cells

To determine whether low oxygen environments enhance cardiac cell division in the neonatal period, newborn rat pups were reared for 21 days in 12-15% oxygen. Left ventricle and right ventricle weights were 30 and 180% greater than controls matched for body weight (P less than 0.001) as were left ventricle/body weight ratios (3.68+/-0.26 vs. 2.99+/-0.05 mg LV/g body wt,P less than 0.001). Left ventricular total DNA and DNA concentration was 95 and 48% greater than controls (P less than 0.001). Autoradiography confirmed that this increase in ventricular DNA resulted from an increased rate of division of cardiac muscle cells, fibroblast, and vascular endothelial cells. When [3H]thymidine was injected on day ), autoradiographs prepared on day 21 reflected an increased dilution of label in hypoxic rats consistent with enhanced proliferation. The labeling index and grains per nucleus of ventricular muscle cells was 25% (P less than 0.01) and 20% (P less than 0.02) less than controls, Thus, hypoxic stress applied early in the neonatal period augments the rate of division and ultimate number of cardiac muscle cells. Whether this enhancement results from a primary effect of oxygen or from secondary hemodynamic factors remains unknown.

Fine Structure of Cardiac Muscle Cells after Injection of Normal and Thiouracil-Treated Rats with Triiodothyronine.

1975 ◽  
Vol 33 ◽  
pp. 536-537
Author(s):  
Eladio A. Nunez ◽  
Martin Hagopian ◽  
Roger L. Greif ◽  
Michael D. Gershon
Keyword(s):  
Drinking Water ◽  
Fine Structure ◽  
Thyroid Hormones ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Left Ventricular ◽  
Ventricular Muscle ◽  
Cardiac Muscle Cells ◽  
Mitochondrial Number ◽  
Morphologic Changes

It has been reported that morphologic changes occur in mitochondria of cardiac muscle cells following treatment with thyroid hormones (thyroxine, triiodothyronine). These observations have been used to support the view that under normal conditions, thyroid hormones control mitochondrial metabolism. We have examined the effect of triiodothyronine on the fine structure of cardiac muscle from normal and thiouracil-treated rats. Rats were given thiouracil (0.1 percent in drinking water) for 10 weeks. Normal and thiouracil-treated rats were injected with triiodothyronine (75 ug of triiodo-L-thyronine i.p. per day) for three days. The left ventricular muscle of normal rats, and rats given thiouracil, triiodothyronine or thiouracil followed by triiodothyronine was examined ultrastructurally. Morphometric analysis of electron micrographs showed that mitochondrial number was not significantly different in the four groups of animals. The fine structure of normal cardiac muscle is illustrated in figure 1. Thiouracil treatment did not alter the fine structure of cardiac muscle cells (Fig. 3).

Cardiocyte contractile performance in experimental biventricular volume-overload hypertrophy

1993 ◽  
Vol 264 (5) ◽  
pp. H1615-H1623 ◽  
Author(s):  
Y. Urabe ◽  
Y. Hamada ◽  
F. G. Spinale ◽  
B. A. Carabello ◽  
R. L. Kent ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Contractile Function ◽  
Volume Overload ◽  
Fold Increase ◽  
Muscle Cells ◽  
Diffraction Measurement ◽  
Cardiac Muscle Cells ◽  
Significant Difference ◽  
Feline Model ◽  
Contractile Performance

Previous studies have shown that the right ventricle (RV) appears to tolerate volume overloading better than does the left ventricle (LV). To determine whether this dichotomous response is due to intrinsic differences in the contractile performance of volume hypertrophied RV vs. LV cardiac muscle cells, or cardiocytes, we characterized the contractile performance of cardiocytes isolated from an experimental feline model of biventricular volume overload (n = 7 cats), wherein a peripheral arteriovenous fistula (AVF) produced an identical duration and degree of volume overload for both ventricles; sham-operated cats served as the appropriate controls (n = 7). Cardiocyte contractile function was defined by laser diffraction measurement of sarcomere motion. For the AVF cats, there was a 2.4-fold increase in cardiac output, a significant increase in the RV and LV weight-to-body weight ratios, and a significant increase in cell surface area for the RV and LV cardiocytes. Despite this, cardiocyte contractile function in the AVF cats was entirely normal. Thus there was no significant difference between RV and LV cardiocytes from control cats in the extent or velocity of sarcomere shortening either in 1 cP superfusate or in higher viscosity superfusates, and comparison of RV and LV cells from the AVF cats to those from sham-operated cats again revealed no significant differences. Furthermore, cardiocyte relengthening properties showed no significant differences between AVF and control groups. In summary, this study shows that contractile dysfunction is not an inherent property of either RV or LV cardiac muscle cells hypertrophying in response to substantial volume overloading when preload is increased but afterload is normal.

scholarly journals Inhibition of p66ShcA redox activity in cardiac muscle cells attenuates hyperglycemia-induced oxidative stress and apoptosis

2009 ◽  
Vol 296 (2) ◽  
pp. H380-H388 ◽  
Author(s):  
Ashwani Malhotra ◽  
Himanshu Vashistha ◽  
Virendra S. Yadav ◽  
Michael G. Dube ◽  
Satya P. Kalra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome C ◽  
Cardiac Muscle ◽  
Ventricular Myocytes ◽  
Muscle Cells ◽  
Molecular Switch ◽  
Left Ventricular ◽  
Cardiac Muscle Cells ◽  
Rat Ventricular Myocytes ◽  
Adult Rat

Apoptotic myocyte cell death, diastolic dysfunction, and progressive deterioration in left ventricular pump function characterize the clinical course of diabetic cardiomyopathy. A key question concerns the mechanism(s) by which hyperglycemia (HG) transmits danger signals in cardiac muscle cells. The growth factor adapter protein p66ShcA is a genetic determinant of longevity, which controls mitochondrial metabolism and cellular responses to oxidative stress. Here we demonstrate that interventions which attenuate or prevent HG-induced phosphorylation at critical position 36 Ser residue (phospho-Ser36) inhibit the redox function of p66ShcA and promote the survival phenotype. Adult rat ventricular myocytes obtained by enzymatic dissociation were transduced with mutant-36 p66ShcA (mu-36) dominant-negative expression vector and plated in serum-free media containing 5 or 25 mM glucose. At HG, adult rat ventricular myocytes exhibit a marked increase in reactive oxygen species production, upregulation of phospho-Ser36, collapse of mitochondrial transmembrane potential, and increased formation of p66ShcA/cytochrome- c complexes. These indexes of oxidative stress were accompanied by a 40% increase in apoptosis and the upregulation of cleaved caspase-3 and the apoptosis-related proteins p53 and Bax. To test whether p66ShcA functions as a redox-sensitive molecular switch in vivo, we examined the hearts of male Akita diabetic nonobese (C57BL/6J) mice. Western blot analysis detected the upregulation of phospho-Ser36, the translocation of p66ShcA to mitochondria, and the formation of p66ShcA/cytochrome- c complexes. Conversely, the correction of HG by recombinant adeno-associated viral delivery of leptin reversed these alterations. We conclude that p66ShcA is a molecular switch whose redox function is turned on by phospho-Ser36 and turned off by interventions that prevent this modification.

THE EFFECTS OF ACUPUNCTURE ON CARDIAC MUSCLE CELLS AND BLOOD PRESSURE IN SPONTANEOUS HYPERTENSIVE RATS

2004 ◽  
Vol 29 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Hung-Chien Wu ◽  
Jaung-Geng Lin ◽  
Chun-Hsien Chu ◽  
Yung-Hsien Chang ◽  
Chung-Gwo Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Hypertensive Rats ◽  
Cardiac Muscle Cells
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