Wyniki wyszukiwania

1

Potassium channel openers and the expression of BCL-type proteins in cardiac myocytes

100%

Kicinska A., Szewczyk A.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

2

Temperature dependent contribution of Ca2+ transporters to relaxation in cardiac myocytes: important role of sarcolemmal Ca2+ -ATPase

88%

Mackiewicz U., Lewartowski B.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 1

Activities of Ca2+-ATPase of sarcoplasmic reticulum (SERCA) and Na+/Ca2+ exchanger (NCX) involved in cellular Ca2+ turnover greatly change in hypertrophied and failing hearts. Unfortunately, contribution of these proteins as well as of the sarcolemmal Ca2+-ATPase (PMCA) to cellular Ca2+ turnover has been investigated almost exclusively at room temperature. PMCA is of particular interest since it may affect activity of calcineurin and nNOS. Therefore the objective of this study was to reinvestigate contribution of SERCA, NCX and PMCA to cell relaxation and the effect of PMCA on cell contraction at 37°C. Myocytes isolated from the ventricles of guinea pig and rat hearts and incubated with Indo-1 were field stimulated at the rate of 60/min. Contribution of SERCA, NCX and PMCA was calculated from the rate constants of the decaying components of electrically stimulated Ca2+ transients or of the transients initiated by caffeine dissolved in normal Tyrode or in 0Na, 0Ca Tyrode. Increase in temperature from 24 to 37°C increased the relative contribution of NCX from 6.1% to 7.5% in rat and from 21.3 to 51.9 % in guinea pig at the expense of SERCA. The contribution of the PMCA to relaxation in both species increased upon rise in temperature from 24 % to 37°C from negligible values to 3.7 %. In both species amplitude of Ca2+ transients was at 24°C nearly twice as high as at 37°C. It was nearly doubled by carboxyeosine (CE), a PMCA blocker at 37°C but was hardly affected at 24°C. The effects of CE were concentration-dependent and conformed with the degree of inhibition of activity of PMCA. Conclusions: PMCA plays an important role in regulation of myocardial contraction despite its small contribution to relaxation. In guinea pig but not in rat relative contribution of SERCA and NCX to relaxation is highly temperature dependent.

3

Upregulation of GRP78 and caspase-12 in diastolic failing heart

75%

Sun Y., Liu G., Song T., Liu F., Kang W., Zhang Y., Ge Z.

Acta Biochimica Polonica

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2008

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tom 55

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nr 3

511-516

Background: The endoplasmic reticulum (ER) fulfills multiple cellular functions. Various stimuli can potentially cause ER stress (ERS). ERS is one of the intrinsic apoptosis pathways and apoptosis plays a critical role in hypertension. Glucose regulated protein 78 (GRP78) has been widely used as a marker for ERS and caspase-12 mediated apoptosis was a specific apoptotic pathway of ER. The expression of GRP78 and caspase-12 remains poorly understood in the diastolic heart failure resulting from hypertension. Methods: We used spontaneously hypertensive rats (SHRs) to establish a model of diastolic heart failure, and performed immunohistochemistry, Western blot, and real-time PCR to analyze GRP78 and caspase-12. Results: We found that GRP78 and caspase-12 had enhanced expression at protein and mRNA levels. Conclusions: These results suggest that GRP78 and caspase-12 were upregulated in cardiomyocytes and ERS can contribute to cardiac myocyte apoptosis in the diastolic heart failure resulting from hypertension.

4

Voltage dependent activation of tonic contraction in cardiac myocytes

75%

Mackiewicz U., Emanuel K., Lewartowski B.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

Contractions of isolated single myocytes of guinea pig heart stimulated by rectangular depolarizing pulses consist of a phasic component and a voltage dependent tonic component. In this study we analyzed the mechanism of activation of the graded, sustained contractions elicited by slow ramp depolarization and their relation to the components of contractions elicited by rectangular depolarizing pulses. Experiments were performed at 37°C in ventricular myocytes of guinea pig heart. Voltage-clamped myocytes were stimulated by the pulses from the holding potential of -40 to +5 mV or by ramp depolarization shifting voltage within this range within 6 s. [Ca2+]i was monitored as fluorescence of Indo 1-AM and contractions were recorded with the TV edge-tracking system. Myocytes responded to the ramp depolarization between -25 and -6 mV by the slow, sustained increase in [Ca2+]i and shortening, the maximal amplitude of which was in each cell similar to that of the tonic component of Ca2+ transient and contraction. The contractile responses to ramp depolarization were blocked by 200 µM ryanodine and Ca2+-free solution, but were not blocked by 20 µM nifedipine or 100 - 200 µM Cd2+ and potentiated by 5 mM Ni2+. The responses to ramp depolarization were with this respect similar to the tonic but not to the phasic component of contraction: both components were blocked by 200 µM ryanodine, and were not blocked by Cd2+ or Ni2+ despite complete inhibition of the phasic Ca2+ current. However, the phasic component but not the tonic component of contraction in cells superfused with Ni2+ was inhibited by nifedipine. Both components of contraction were inhibited by Ca2+-free solution superfused 15 s prior to stimulation. Conclusions: In myocytes of guinea pig heart the contractile response to ramp depolarization is equivalent to the tonic component of contraction. It is activated by Ca2+ released from the sarcoplasmic reticulum by the ryanodine receptors. Their activation and inactivation is voltage dependent and it does not depend on the Ca2+ influx by the Ca2+ channels or reverse mode Na+/Ca2+ exchange, however, it may depend on Ca2+ influx by some other, not yet defined route.

5

Effects of thapsigargin on stimulation frequency - dependent changes in mitochondrial calcium in rat cardiac myocytes

75%

Pytkowski B., Lewartowski B.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,2

We investigated in the single myocytes of rat heart the effect of blocking of ATP-ase of sarcoplasmic reticulum (SR) on mitochondrial Ca2+ uptake and release. Mitochondrial Ca2+ content was investigated as Mn2+ - resistant fluorescence of Indo 1 - AM loaded into cells. SR ATP-ase was blocked with 10-6 M thapsigargin (Tg). Tg blocked almost completely stimulation Œdependent mitochondrial Ca2+ uptake and slowed down its release despite that the maximal cytosolic Ca2+ concentration was not decreased. We propose that mitochondrial stimulation -dependent Ca2+ uptake is greatly enhanced by [Ca2+ ] built by SR in microdomains adjacent to these organelle.

6

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Dihydropyridine receptors functioning as voltage sensors in cardiac myocytes

75%

Mackiewicz U., Emanuel K., Lewartowski B.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 4,2

7

The source of contracticle calcium in guinea-pig cardiac myocytes treated with thapsigargin

75%

Janiak R., Lewartowski B.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 3

8

Altered expression of adenosine receptors in heart of diabetic rat

63%

Grden M., Podgorska M., Szutowicz A., Pawelczyk T.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 4

Diabetes results in functional, biochemical, and morphological abnormalities in the heart. Some of these changes may be attributed to altered adenosine action. This study aimed to examine the expression level of adenosine receptors (AR) in heart of streptozotocin-induced diabetic rat. Performed analyses revealed detectable levels of A1-AR, A2a-AR, A2b-AR, A3-AR mRNA and protein in whole heart and isolated cardiac myocytes. An increase in A1-AR protein content with no changes in mRNA level was observed in isolated cardiac myocytes. Diabetes resulted in an increase of A3-AR mRNA and protein levels in heart and in cardiac myocytes. The level of A2a-AR mRNA was increased in whole diabetic heart, but it decreased in cardiac myocytes with no detectable changes in protein content. We did not observe any changes in expression level of A2b-AR in diabetic heart and isolated cardiac myocytes. Administration of insulin to diabetic rat for four days resulted in returning of the ARs mRNA and protein to the levels observed in heart of normal rat. These changes in ARs genes expression, and receptors protein content correspond to some abnormalities characteristic of the diabetic heart, suggesting involvement in pathogenesis of diabetic cardiomyopathy.

9

Myocardial necrosis due to vitamin D3 overdose - scanning electron microscopic observations

63%

Walentynowicz O., Kubasik-Juraniec J., Rudzinska-Kisiel T.

Folia Morphologica

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2004

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tom 63

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nr 4

Our studies were carried out on the hearts of virgin female Wistar rats treated with 100.000 i.u. of vitamin D₃ (calciol) per os for 3 consecutive days. Multifocal cardionecrosis was established macroscopically in 70% of the vitamin D-treated rats on the 7th day of the experiment when the rats were in the acute phase of intoxication. Using a scanning electron microscopy (SEM), we received three-dimensional information about the structural changes to the rat myocardium damaged by high doses of vitamin D₃. The images of necrotic hearts revealed significant disruption of the structural integrity of the myocardium linked to fragmentation of the cardiac muscle bundles and a visible disruption of the extracellular matrix (ECM) components. In healthy hearts, the structural integrity of the myocardium and the dense network of the extracellular matrix were well preserved. In parallel, the effect of an increasing concentration of free Ca²⁺ on the total proteolytic activity of the heart muscle homogenate of the healthy and necrotic rats was investigated at neutral pH. These data showed that following vitamin D₃ intoxication, the proteolytic processes in the rat hearts occurred in Ca²⁺ overload or saturation. On the basis of our morphological and biochemical results we can suggest that calcium-activated neutral proteinases may have contributed to the structural alteration of the extracellular matrix components and were in this way involved in vitamin D-induced cardionecrosis.

10

Agonist of dihydropyridine receptors, BayK8644 depresses excitation-contraction coupling in myocytes of guinea pig heart

63%

Mackiewicz U., Emanuel K., Lewartowski B.

Journal of Physiology and Pharmacology

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2001

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tom 52

|

nr 3

11

Requirements for the localization of p130 Cas to Z-lines in cardiac myocytes

63%

Kovacic-Milivojevic B., Damsky C. C., Gardner D. G., Ilic D.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr 2

The vertebrate heart responds to hemodynamic load with the enlargement of postmitotic, terminally differentiated cardiac myocytes. Such hypertrophic changes are characterized by alterations in sarcomeric organization and gene expression. Previously, we established a role for a nonreceptor tyrosine kinase, focal adhesion kinase, in signaling the changes in cytoskeletal organization associated with hypertrophy [1], Here, we report on data supporting a key role for p130Cas in this process. In neonatal cardiac myocytes FAK, Cas and paxillin are located in sarcomeric Z-lines, suggesting that the Z-line is an important signaling locus in these cells. The expression of different Cas mutants results in a nearly complete loss of sarcomeric organization in these myocytes. Moreover, expression of the C-terminal focal adhesion-targeting domain of FAK both disrupted sarcomeric organization and interfered with the localization of endogenous Cas to Z-lines. These findings suggest that the association of FAK and Cas and the preservation of multiple protein-interaction motifs of Cas are required for the correct assembly of sarcomeres in cardiac myocytes.

12

Thapsigargin inhibits the effects of noradrenaline and high [Ca2]0 on kinetics but not on amplitude of contraction in the single myocytes of guinea pig heart

63%

Janiak R., Lewartowski B.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 1

13

Apoptosis and some of its medical implications

63%

Kawiak J., Hoser G., Skorski T.

Folia Histochemica et Cytobiologica

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1998

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tom 36

|

nr 3

14

Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in c-kit positive cells during development of cardiac hypertrophy

51%

Ocsan R. J., Lai Y. N., Prabhu K. V., Hambly B. D., McLachlan

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 6

15

Neutrophils-induced increase of adenosine triphosphate depletion in rat neonatal cardiac myocytes with impaired energy metabolism

51%

Gajewski M., Laskowska-Bozek H., Maslinski S., Ryzewski J.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 4

Isolated, cultured rat neonatal cardiac myocytes were placed in medium suppled menfed with mitochondrial respiratory inhibitor potassium cyanide which caused a rapid adenosine triphosphate (ATP) depletion. These myocytes with the impaired energy metabolism (“hypoxia-like state”) were exposed to unstimulated human neutrophils. Effect of human neu rophils on the myocy es m the “hypoxia-like state” was quantified as a total change in the amount of ATP in cardiac cells. After 5 hours of incubation of neu rophils with the myocytes in the “hypoxia-like state” an additional decrease (of 50 per cent) in ATP content was observed. Since catalase (which destroys hydrogen peroxide) prevented the further decline in ATP level in the myocy es with impaired energy metabolism, it seem that hydrogen peroxide and possibly their products are responsible for this effect. These results suggest that unstimulated human neu rophils af er activation by the contact with injured cardiac cells caused further decrease of ATP level in target cells.

16

Effect of sarcoplasmic reticulum Ca release into diadic region on Na-Ca exchange in cardiac myocytes

51%

Lewartowski B., Janiak R., Langer G. A.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 4

17

Dibucaine displaceable sarcolemmal Ca2 plus fraction in guinea-pig cardiac myocytes

51%

Lewartowski B., Emanuel K., Langer G. A.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 2

18

Effects of mibefradil, a blocker of T-type Ca2plus channels, in single myocytes and intact muscle of guinea-pig heart

51%

Emanuel K., Mackiewicz U., Pytkowski B., Lewartowski B.

Journal of Physiology and Pharmacology

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1998

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tom 49

|

nr 4

19

Effect of Na current on excitation-contraction coupling in ventricular myocytes of guinea pig heart

51%

Janiak R., Lewartowski B.

Journal of Physiology and Pharmacology

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1997

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tom 48

|

nr 2

20

Coronary vascular endothelium-myocyte interactions in protection of the heart by ischaemic preconditioning

51%

Parratt J. R., Vegh A.

Journal of Physiology and Pharmacology

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1999

|

tom 50

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nr 4

Ograniczanie wyników

Potassium channel openers and the expression of BCL-type proteins in cardiac myocytes

Temperature dependent contribution of Ca2+ transporters to relaxation in cardiac myocytes: important role of sarcolemmal Ca2+ -ATPase

Upregulation of GRP78 and caspase-12 in diastolic failing heart

Voltage dependent activation of tonic contraction in cardiac myocytes

Effects of thapsigargin on stimulation frequency - dependent changes in mitochondrial calcium in rat cardiac myocytes

Dihydropyridine receptors functioning as voltage sensors in cardiac myocytes

The source of contracticle calcium in guinea-pig cardiac myocytes treated with thapsigargin

Altered expression of adenosine receptors in heart of diabetic rat

Myocardial necrosis due to vitamin D3 overdose - scanning electron microscopic observations

Agonist of dihydropyridine receptors, BayK8644 depresses excitation-contraction coupling in myocytes of guinea pig heart

Requirements for the localization of p130 Cas to Z-lines in cardiac myocytes

Thapsigargin inhibits the effects of noradrenaline and high [Ca2]0 on kinetics but not on amplitude of contraction in the single myocytes of guinea pig heart

Apoptosis and some of its medical implications

Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in c-kit positive cells during development of cardiac hypertrophy

Neutrophils-induced increase of adenosine triphosphate depletion in rat neonatal cardiac myocytes with impaired energy metabolism

Effect of sarcoplasmic reticulum Ca release into diadic region on Na-Ca exchange in cardiac myocytes

Dibucaine displaceable sarcolemmal Ca2 plus fraction in guinea-pig cardiac myocytes

Effects of mibefradil, a blocker of T-type Ca2plus channels, in single myocytes and intact muscle of guinea-pig heart

Effect of Na current on excitation-contraction coupling in ventricular myocytes of guinea pig heart

Coronary vascular endothelium-myocyte interactions in protection of the heart by ischaemic preconditioning