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A poly[ADP-ribose] synthetase inhibitor, benzamide protects smooth muscle cells but not endothelium against ischemia-reperfusion injury in isolated guinea-pig heart

100%
Jakubowski A., Lomnicka M.
Acta Biochimica Polonica
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2007
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tom 54
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nr 1
Activation of the nuclear enzyme poly(ADP-ribose) synthethase (PARS) is important in the cellular response to oxidative stress. During ischemia and reperfusion (I/R) increased free radical production leads to DNA breakage that stimulates PARS which in turn results in an energy-consuming metabolic cycle and initiation of the apoptotic process. Previous studies have reported that PARS inhibition confers protection in various models of I/R-induced cardiovascular damage. The purpose of this study was to determine the role of PARS inhibition in I/R-induced injury of smooth muscle cells and endothelium in the coronary circulation of the isolated guinea-pig heart. Control hearts and those treated with a PARS inhibitor — benzamide (100 µmol L-1), were subjected to 30 min of subglobal ischemia and subsequent reperfusion (90 min). To analyze the functional integrity of smooth muscle cells and endothelium, one-minute intracoronary infusions of endothelium-independent (sodium nitroprusside, NaNP; 3 µmol L-1) and endothelium-dependent (substance P, SP; 10 nmol L-1) vasodilators were used before ischemia and at the reperfusion time. The degree of the injury of coronary smooth muscle and endothelial cells induced by I/R was estimated in terms of diminished vasodilator responses to NaNP (at 55 min and 85 min of reperfusion) and to SP (at 70 min of reperfusion), respectively, and expressed as the percentage of preischemic response. I/R reduced vasorelaxant responses to both vasodilators by half (to 54.1 ± 5.1% and to 53.6 ± 4.9% of preischemic value for NaNP at 55 min and 85 min of reperfusion, respectively and to 45.9 ± 6.5% for SP at 70 min of reperfusion). PARS inhibition provided complete restoration of vasorelaxation induced by NaNP (107.6 ± 13.3% and 104 ± 14.4% of preischemic response at the two time points of reperfusion, respectively). However, there was no effect on the SP-induced response (48+12.1% of preischemic response). We conclude that pharmacological PARS inhibition with benzamide protects coronary smooth muscle cells but not endothelium against I/R-induced reperfusion injury in the coronary circulation of the guinea-pig heart.
2
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Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning

80%
Chlopicki S., Lomnicka M., Gryglewski R. J.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 4
3
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The involvement of adhesion molecules and lipid mediators in the adhesion of human platelets to eosinophils

80%
Jawien J., Lomnicka M., Korbut R., Chlopicki S.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
Platelet-leukocyte interactions represent an important determinant of the inflammatory response. Although mechanisms of platelet-neutrophil adhesion were studied extensively, little is known on the mechanisms of platelet-eosinophil interactions. The aim of the present study was to analyze the involvement of adhesion molecules and lipid mediators in platelet-eosinophil adhesion as compared to platelet-neutrophil adhesion. For that purpose human platelets, eosinophils and neutrophils were isolated and platelet-eosinophil and platelet-neutrophil adhesion induced by thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) was quantified using the "rosettes" assay. The involvement of adhesion molecules such as selectin P, glycoprotein IIb/IIIa (GPIIb/IIIa) and lipid mediators such as of thromboxane A2 (TXA2), platelet activating factor (PAF) and cysteinyl leukotrienes (cysLTs) were studied using monoclonal antibodies and pharmacological inhibitors, respectively. Thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) each of them induced platelet-eosinophil adhesion that was even more pronounced as compared with platelet-neutrophil adhesion induced by the same stimulus. Anti-CD62P antibody (1 µg/ml) and anti-GP IIb/IIIa antibody (abciximab - 3 µg/ml) strongly inhibited platelet-eosinophil as well as platelet-neutrophil adhesion. Aspirin inhibited platelet-eosinophil adhesion, while MK 886 - a FLAP inhibitor (10 µM), or WEB 2170 - a PAF receptor antagonist (100 µM) were less active. On the other hand aspirin, MK 886 and WEB 2170 all three of them inhibited platelet-neutrophil adhesion. In summary, platelets adhered avidly to eosinophils both after activation of platelets by thrombin, eosinophils by fMLP or simultaneous activation of platelets and eosinophils by LPS. Similarly to platelet-neutrophil interaction adhesion of platelets to eosinophils involved not only adhesion molecules (selectin P, GPIIb/IIIa), but also lipid mediators such as TXA2. The involvement of PAF and cysteinyl leukotrienes in platelet-eosinophil adhesion was less pronounced as compared to platelet-neutrophil adhesion.
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