Rigor tension in single skinned rat cardiac cell: role of myofibrillar creatine kinase

The influence of phosphocreatine in the presence or absence of MgATP and MgADP was studied in Triton X-100-treated thin papillary muscles and ventricular strips of the rat heart. The pCa/tension relationships, the pMgATP/tension relationships, and the tension responses to quick length changes were analyzed. The results show three major consequences of the reduction of the phosphocreatine concentration in the presence of millimolar concentrations of the MgATP. (a) The resting tension and the maximal Ca2+-activated tension were increased, and the pCa/tension relationship was shifted toward higher pCa values and its steepness was decreased; these effects were enhanced by the inclusion of MgADP. (b) The time constant of tension recoveries after quick stretches applied during maximal activation was increased, while the extent of these recoveries was decreased. (c) The study of pMgATP/tension relationships in low Ca concentrations showed that the decrease in phosphocreatine induced a shift toward higher MgATP values with no changes in maximal rigor tension or the slope coefficient; these effects were increased by the increase in MgADP and were independent of the preparation diameter. Thus, modifications of the apparent Ca sensitivity and resting and maximal tension when phosphocreatine is decreased seem to be due to an increasing participation of rigor-like or slowly cycling cross-bridges spending more time in the attached state. These results suggest that endogenous creatine kinase is able to ensure maximal efficiency of myosin ATPase by producing a local high MgATP/MgADP ratio.

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Role of transesophageal echocardiography in the assessment of patients with blunt chest trauma: Correlation of echocardiographic findings with the electrocardiogram and creatine kinase monoclonal antibody measurements

American Heart Journal ◽

10.1016/s0002-8703(98)70324-2 ◽

1998 ◽

Vol 135 (3) ◽

pp. 476-481 ◽

Cited By ~ 56

Author(s):

Miguel A. García-Fernández ◽

José M. López-Pérez ◽

Nicasio Pérez-Castellano ◽

Lorenzo F. Quero ◽

Alejandro Virgós-Lamela ◽

...

Keyword(s):

Monoclonal Antibody ◽

Creatine Kinase ◽

Transesophageal Echocardiography ◽

Blunt Chest Trauma ◽

Chest Trauma ◽

Echocardiographic Findings

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Abstract 26: Fibroblast Growth Factor 21 Prevents Diabetic Cardiomyopathy by Attenuating Cardiac Lipotoxicity via Erk1/2-dependent Signaling Pathway in Mice

Circulation Research ◽

10.1161/res.117.suppl_1.26 ◽

2015 ◽

Vol 117 (suppl_1) ◽

Author(s):

Yi Tan ◽

Chi Zhang ◽

Xiaoqing Yan ◽

Zhifeng Huang ◽

Junlian Gu ◽

...

Keyword(s):

Cell Death ◽

Type 1 Diabetes ◽

Signaling Pathway ◽

P38 Mapk ◽

Diabetic Cardiomyopathy ◽

Cardiac Cell ◽

Diabetic Mice ◽

Ampk Signaling

The role of FGF21 plays in the development and progression of diabetic cardiomyopathy (DCM) has not been addressed. Here we demonstrated that type 1 diabetes decreased FGF21 levels in the blood, but up-regulated cardiac fgf21 expression about 40 fold at 2 months and 3-1.5 fold at 4 and 6 months after diabetes, which indicated a cardiac specific FGF21 adaptive up-regulation. To define the critical role of FGF21 in DCM, type 1 diabetes was induced in FGF21 knock out (FGF21KO) mice. At 1, 2 and 4 months after diabetes onset, no significant differences between FGF21KO and wild type (WT) diabetic mice in blood glucose and triglyceride levels were observed. But FGF21KO diabetic mice showed earlier and more severe cardiac dysfunction, remodeling and oxidative stress, as well as greater increase in cardiac lipid accumulation than WT diabetic mice. Mechanistically, FGF21 reduced palmitate-induced cardiac cell death, which was accompanied by up-regulation of cardiac Erk1/2, p38 MAPK and AMPK phosphorylation. Inhibition of each kinase with its inhibitor and/ or siRNA revealed that FGF21 prevents palmitate-induced cardiac cell death via up-regulating the Erk1/2-dependent p38 MAPK/AMPK signaling pathway. In vivo administration of FGF21, but not FGF21 plus ERK1/2 inhibitor, to diabetic mice significantly prevented cardiac cell death and reduced inactivation of Erk1/2, p38 MAPK and AMPK, and prevented cardiac remodeling and dysfunction at late-stage. Our results demonstrate that cardiac FGF21 decompensation may contribute to the development of DCM and FGF21 may be a therapeutic target for the treatment of diabetic cardiac damage via activation of Erk1/2-P38 MAPK-AMPK signaling.

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Role of creatine and creatine kinase in UCP1-independent adipocyte thermogenesis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00367.2020 ◽

2020 ◽

Vol 319 (5) ◽

pp. E944-E946 ◽

Cited By ~ 1

Author(s):

Theo Wallimann ◽

Malgorzata Tokarska-Schlattner ◽

Laurence Kay ◽

Uwe Schlattner

Keyword(s):

Creatine Kinase

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Adaptation of cardiac myosin and creatine kinase to chronic hypoxia: role of anorexia and hypertension

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.4.h1690 ◽

1997 ◽

Vol 272 (4) ◽

pp. H1690-H1695 ◽

Cited By ~ 5

Author(s):

M. Pissarek ◽

X. Bigard ◽

P. Mateo ◽

C. Y. Guezennec ◽

J. A. Hoerter

Keyword(s):

Pulmonary Hypertension ◽

Creatine Kinase ◽

Hypobaric Hypoxia ◽

Chronic Hypoxia ◽

Specific Activity ◽

Cardiac Myosin ◽

Simulated Altitude ◽

Biochemical Basis ◽

Threefold Increase

The effects of chronic hypobaric hypoxia (CHH, 28 days, simulated altitude 5,500 m) on the cardiac expression of myosin heavy chain (MHC) and creatine kinase (CK) was studied in rat left (LV) and right (RV) ventricle. To separate the effects of hypoxia from its associated perturbations, anorexia and pulmonary hypertension (resulting in RV hypertrophy), CHH animals were compared with normoxic controls (C) and with rats restricted in food supply (pair fed, PF). In RV, the increased proportion of beta-MHC in CHH (20 +/- 3%) vs. C (7 +/- 2%, P < 0.01) and vs. PF (12 +/- 2%, P < 0.05) rats was mainly attributed to hypertension. In contrast, the higher beta-MHC of CHH (23 +/- 2%) vs. C (13 +/- 2%, P < 0.05) in LV was mainly ascribed to anorexia (PF = 21 +/- 3%, not significant). A major contribution of anorexia was also evidenced in the isozymic profile of CK; anorexia accounted for a 25% decrease in mito-CK specific activity in LV, whereas hypertension partly accounted for the threefold increase in BB-CK in RV. CHH specifically induced a twofold rise in LV BB-CK. This suggests that both the expression of slow myosin, improving the economy of contraction, and the changes in CK isozymic profile could provide a biochemical basis for the CHH resistance to ischemia.

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Velocity of the creatine kinase reaction in the neonatal rabbit heart: role of mitochondrial creatine kinase

Biochemistry ◽

10.1021/bi00406a052 ◽

1988 ◽

Vol 27 (6) ◽

pp. 2165-2172 ◽

Cited By ~ 47

Author(s):

Stanton B. Perry ◽

John McAuliffe ◽

James A. Balschi ◽

Paul R. Hickey ◽

Joanne S. Ingwall

Keyword(s):

Creatine Kinase ◽

Rabbit Heart ◽

Mitochondrial Creatine Kinase ◽

Kinase Reaction ◽

Creatine Kinase Reaction

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Contraction-induced injury to the extensor digitorum longus muscles of rats: the role of vitamin E

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.3.817 ◽

1997 ◽

Vol 83 (3) ◽

pp. 817-823 ◽

Cited By ~ 34

Author(s):

Jack H. Van Der Meulen ◽

Anne McArdle ◽

Malcolm J. Jackson ◽

John A. Faulkner

Keyword(s):

Creatine Kinase ◽

Vitamin E ◽

Pyruvate Kinase ◽

Extensor Digitorum Longus ◽

Muscle Fibers ◽

Extensor Digitorum ◽

Intravenous Injections ◽

Antioxidant Function ◽

The Difference

Van der Meulen, Jack H., Anne McArdle, Malcolm J. Jackson, and John A. Faulkner. Contraction-induced injury to the extensor digitorum longus muscles of rats: the role of vitamin E. J. Appl. Physiol. 83(3): 817–823, 1997.—Three days after a protocol of 225 pliometric (lengthening) contractions was administered to in situ extensor digitorum longus muscles of rats, the force deficit was 64 ± 7% and the percentage of damaged muscle fibers was 38 ± 5% of the control values. We then tested the hypothesis that at 3 h and 3 days after the protocol an elevation in the muscle vitamin E content would decrease the force deficit, the percentage of damaged muscle fibers, and the serum activities of creatine kinase and pyruvate kinase. The 5–8 days of intravenous injections of α-tocopherol increased muscle vitamin E content threefold compared with vehicle (ethanol)-treated rats. Despite the difference in vitamin E content, the force deficit and number of damaged fibers were not different. After the contraction protocol, the serum creatine kinase and pyruvate kinase activities of the vehicle-treated rats increased fourfold at 3 h and twofold at 3 days, whereas the vitamin E-treated rats showed no change. We conclude that vitamin E treatment did not ameliorate either the induction of the injury or the more severe secondary injury at 3 days. Despite the absence of evidence for an antioxidant function, the lack of any increase in serum enzyme activities for vitamin E-treated rats at 3 h and 3 days supported a role for vitamin E in the prevention of enzyme loss after muscle damage.

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Myofibrillar end of the creatine phosphate energy shuttle

AJP Cell Physiology ◽

10.1152/ajpcell.1984.247.5.c424 ◽

1984 ◽

Vol 247 (5) ◽

pp. C424-C432 ◽

Cited By ~ 24

Author(s):

F. Savabi ◽

P. J. Geiger ◽

S. P. Bessman

Keyword(s):

Creatine Kinase ◽

Adenylate Kinase ◽

Psoas Muscle ◽

Creatine Phosphate ◽

Force Of Contraction ◽

Physiological Concentration ◽

Complete Relaxation ◽

Order Of Magnitude ◽

Contraction And Relaxation

Isometric contraction and relaxation of glycerinated rabbit psoas muscle fibers containing native creatine kinase (CK) and ATPase activities were studied. Energy for contraction and relaxation was provided either by ADP + creatine phosphate (CP) or ATP alone, and the effectiveness of these additions on rate and maximum force of contraction and relaxation were compared. In the presence of 250 microM ADP, physiological concentration of CP (10 mM) produced faster and stronger contraction and faster and more complete relaxation than equimolar or even higher concentrations of ATP. When contraction was initiated by addition of ADP to fibers preincubated with 10 mM CP, the apparent Km for ADP was 1.18 +/- 0.24 mM. If the fibers were preincubated with ADP and contraction initiated by addition of 10 mM CP, the apparent Km for ADP was more than an order of magnitude smaller (76.0 +/- 4 microM). The observed Km for ADP for contraction was about half the Km for CP in solution (151.5 microM). The apparent Km for CP for rate of contraction was 2.67 +/- .046 mM independent of sequence of addition of ADP. Since these experiments were done in the presence of P1,P5-diadenosine 5'-pentaphosphate, a powerful inhibitor of adenylate kinase, the role of this enzyme in the process was not significant. These observations support the idea of compartmentation of myofibrillar CK in close function with myosin ATPase as part of the phosphoryl creatine energy shuttle.

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