IGF1 Activates PKC α-Dependent Protein Synthesis in Adult Rat Cardiomyocytes

2000 ◽  
Vol 4 (3) ◽  
pp. 166-171 ◽  
Author(s):  
Anna Pecherskaya ◽  
Michele Solem
Keyword(s):  
Protein Synthesis ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Dependent Protein

scholarly journals Ca+2/Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Rong-Huai Zhang ◽  
Haitao Guo ◽  
Machender R. Kandadi ◽  
Xiao-Ming Wang ◽  
Jun Ren
Keyword(s):  
Kinase Inhibitor ◽  
Maximal Velocity ◽  
Cam Kinase ◽  
Glucose Toxicity ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Cardiac Contractile ◽  
Intracellular Ca ◽  
Dependent Protein ◽  
The Impact

(1) Hyperglycemia leads to cytotoxicity in the heart. Although several theories are postulated for glucose toxicity-induced cardiomyocyte dysfunction, the precise mechanism still remains unclear. (2) This study was designed to evaluate the impact of elevated extracellular Ca2+on glucose toxicity-induced cardiac contractile and intracellular Ca2+anomalies as well as the mechanism(s) involved with a focus on Ca2+/calmodulin (CaM)-dependent kinase. Isolated adult rat cardiomyocytes were maintained in normal (NG, 5.5 mM) or high glucose (HG, 25.5 mM) media for 6-12 hours. Contractile indices were measured including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), and time-to-90% relengthening (TR90). (3) Cardiomyocytes maintained with HG displayed abnormal mechanical function including reduced PS, ±dL/dt, and prolonged TPS, TR90and intracellular Ca2+clearance. Expression of intracellular Ca2+regulatory proteins including SERCA2a, phospholamban and Na+-Ca2+exchanger were unaffected whereas SERCA activity was inhibited by HG. Interestingly, the HG-induced mechanical anomalies were abolished by elevated extracellular Ca2+(from 1.0 to 2.7 mM). Interestingly, the high extracellular Ca2+-induced beneficial effect against HG was abolished by the CaM kinase inhibitor KN93. (4) These data suggest that elevated extracellular Ca2+protects against glucose toxicity-induced cardiomyocyte contractile defects through a mechanism associated with CaM kinase.

cAMP and protein synthesis in isolated adult rat heart preparations

1993 ◽  
Vol 265 (5) ◽  
pp. C1247-C1257 ◽  
Author(s):  
M. A. Bogoyevitch ◽  
S. J. Fuller ◽  
P. H. Sugden
Keyword(s):  
Protein Synthesis ◽  
Protein Kinase ◽  
Rat Heart ◽  
Adenine Nucleotide ◽  
Adrenergic Agonists ◽  
Perfused Heart ◽  
Dependent Protein Kinase ◽  
Adult Rat ◽  
Dependent Protein ◽  
Stimulation Of

The involvement of adenosine 3',5'-cyclic monophosphate (cAMP) in the stimulation of ventricular protein synthesis by aortic hypertension or adrenergic agonists in the adult rat heart was investigated. In either the retrogradely or anterogradely perfused heart, aortic hypertension increased protein synthesis rates by up to 19%. However, no changes in cAMP concentrations or in cAMP-dependent protein kinase activity ratios could be detected either at early (< 5 min) or late (90 min) time points. Although isoproterenol, 3-isobutyl-1-methylxanthine, or forskolin raised cAMP concentrations (by up to 4.5-fold) and cAMP-dependent protein kinase ratios (by up to 4-fold), protein synthesis rates were not increased; however, under some perfusion conditions, glucagon did stimulate protein synthesis by 25%. Epinephrine stimulated protein synthesis by up to 32%, an effect that was not prevented by propranolol. Phenylephrine also stimulated protein synthesis, an effect that was prevented by prazosin but was unaffected by yohimbine. These findings implicate the alpha 1-adrenoceptor in the regulation of cardiac protein synthesis. Because changes in adenine nucleotide concentrations were similar in hearts perfused with epinephrine or with the agents that raised cAMP, it is unlikely that adenine nucleotide depletion is responsible for the failure to observe effects of the latter group of agents on protein synthesis. Although isoproterenol or forskolin raised cAMP concentrations in isolated ventricular cardiomyocytes where ATP depletion was minimal, neither stimulated protein synthesis. alpha 1-Adrenergic agonists stimulate phosphoinositide hydrolysis in the heart (Brown, J. H., I. L. Buxton, and L. L. Brunton. Circ. Res. 57:532-537, 1985). Aortic hypertension doubled the rate of phosphoinositide hydrolysis in the perfused heart. We suggest that the phosphoinositide-linked signal transduction pathway is more likely to be involved in stimulation of cardiac protein synthesis by hypertension or adrenergic agonism than the adenylyl cyclase/cAMP-linked pathway.

Noradrenaline-induced increase in protein synthesis in adult rat cardiomyocytes: involvement of only α 1A -adrenoceptors

2001 ◽  
Vol 364 (5) ◽  
pp. 444-453 ◽  
Author(s):  
Klaus Pönicke ◽  
Klaus-Dieter Schlüter ◽  
Ingrid Heinroth-Hoffmann ◽  
Torsten Seyfarth ◽  
Martina Goldberg ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Rat Cardiomyocytes ◽  
Adult Rat

scholarly journals P2-202: INHIBITION OF ACTIVITY-DEPENDENT PROTEIN SYNTHESIS BY IL-1β IN HIPPOCAMPAL DENDRITES

2019 ◽  
Vol 15 ◽  
pp. P654-P654
Author(s):  
G. Aleph Prieto ◽  
Erica D. Smith ◽  
Liqi Tong ◽  
Michelle Nguyen ◽  
Carl W. Cotman
Keyword(s):  
Protein Synthesis ◽  
Dependent Protein ◽  
Activity Dependent

scholarly journals IP3R1 regulates Ca2+ transport and pyroptosis through the NLRP3/Caspase-1 pathway in myocardial ischemia/reperfusion injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Guixi Mo ◽  
Xin Liu ◽  
Yiyue Zhong ◽  
Jian Mo ◽  
Zhiyi Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Caspase 1 ◽  
Intracellular Ca ◽  
Myocardial Ischemia Reperfusion

AbstractIntracellular ion channel inositol 1,4,5-triphosphate receptor (IP3R1) releases Ca2+ from endoplasmic reticulum. The disturbance of IP3R1 is related to several neurodegenerative diseases. This study investigated the mechanism of IP3R1 in myocardial ischemia/reperfusion (MI/R). After MI/R modeling, IP3R1 expression was silenced in myocardium of MI/R rats to explore its role in the concentration of myocardial enzymes, infarct area, Ca2+ level, NLRP3/Caspase-1, and pyroptosis markers and inflammatory factors. The adult rat cardiomyocytes were isolated and cultured to establish hypoxia/reperfusion (H/R) cell model. The expression of IP3R1 was downregulated or ERP44 was overexpressed in H/R-induced cells. Nifedipine D6 was added to H/R-induced cells to block Ca2+ channel or Nigericin was added to activate NLRP3. IP3R1 was highly expressed in myocardium of MI/R rats, and silencing IP3R1 alleviated MI/R injury, reduced Ca2+ overload, inflammation and pyroptosis in MI/R rats, and H/R-induced cells. The binding of ERP44 to IP3R1 inhibited Ca2+ overload, alleviated cardiomyocyte inflammation, and pyroptosis. The increase of intracellular Ca2+ level caused H/R-induced cardiomyocyte pyroptosis through the NLRP3/Caspase-1 pathway. Activation of NLRP3 pathway reversed the protection of IP3R1 inhibition/ERP44 overexpression/Nifedipine D6 on H/R-induced cells. Overall, ERP44 binding to IP3R1 inhibits Ca2+ overload, thus alleviating pyroptosis and MI/R injury.

Ca2 Mobilization in Adult Rat Cardiomyocytes by Angiotensin Type 1 and 2 Receptors

1998 ◽  
Vol 55 (9) ◽  
pp. 1413-1418 ◽  
Author(s):  
Qiming Shao ◽  
Laura Saward ◽  
Peter Zahradka ◽  
Naranjan S Dhalla
Keyword(s):  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Angiotensin Type

Triiodothyronine restricts myofibrillar growth and enhances beating frequency in cultured adult rat cardiomyocytes

1998 ◽  
Vol 93 (5) ◽  
pp. 391-395 ◽  
Author(s):  
M.C. Schaub ◽  
M.A. Hefti ◽  
B.A. Harder ◽  
H.M. Eppenberger
Keyword(s):  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Beating Frequency
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