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Upregulation of angiotensin AT1a receptors mRNA in the heart and renal medulla after myocardial infarction in rats

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Milik E., Szczepanska-Sadowska E., Cudnoch-Jedrzejewska A., Dobruch J., Morton M., Koperski L.
Journal of Physiology and Pharmacology
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2006
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tom 57
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nr 3
The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 ± 1.8% and to 31.0 ± 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P < 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.
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Expression and function of extracellular matrix metalloproteinase-9 in human epilepsy

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Konopka A., Grajkowska W., Ziemianska K., Roszkowski M., Rysz A., Koperski L., Kaczmarek L., Wilczynski G., Dzwonek J.
Acta Neurobiologiae Experimentalis
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2011
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tom 71
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nr S
Focal cortical dysplasia (FCD) is a developmental brain disorder characterized by abnormalities of cytoarchitecture and neuronal morphology. FCD is associated with pharmacologically intractable forms of epilepsy in both children and adults. The mechanisms that underlie FCD-associated seizures are unclear. It is believed that a pathological plasticity, including abnormality of synaptic connections, plays the crucial role in this disease. Recent studies indicate the role of interactions between nerve cells and the extracellular matrix in the processes of plasticity. Matrix metalloproteinases are enzymes, which are able to degrade the extracellular matrix components, so they can play an important role in these interactions. Results of experiments using rodent models showed that extracellular matrix metalloproteinase-9 (MMP-9) can play an important role in epileptogenesis. There is no data demonstrating that MMP-9 is involved in the development of epilepsy in human. The aim of this study was to determine whether MMP-9 might play a role in FCD - related epilepsy. Expression of MMP-9 was investigated in human brain tissue derived from people suffering from epilepsy. The immunohistochemistry and antibody microarray methods were used. The control group consisted of the autopsy brain samples. The results indicate that the expression of MMP-9 in the human brain tissue with FCD is increased. The highest immunoreactivity occurs in cytoplasm of abnormal neurons. Moreover, among the 7 tested matrix metalloproteinases (MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, MMP-10, MMP-13), MMP-9 is present in greatest concentration in the FCD tissue homogenates. The results support the hypothesis of the possible role of MMP-9 in the development of human epilepsy and give an opportunity to develop new treatments.
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Fluid consumption, electrolyte excretion and heart remodelling in rats with myocardial infartc maintained on regular and high sodium intake

84%
Cudnoch-Jedrzejewska A., Szczepanska-Sadowska E., Dobruch J., Morton M., Koperski L., Wasiutynski A., Wsol A., Kowalewski S.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
The purpose of the study was to determine effect of high sodium intake on fluid and electrolyte turnover and heart remodeling in the cardiac failure elicited by myocardial infarction (MI). The experiments were performed on four groups of Sprague Dawley rats maintained on food containing 0.45% NaCl and drinking either water (groups 1, 2) or 1% NaCl (groups 3, 4). Groups 1 and 3 were sham-operated while in groups 2 and 4 MI was produced by the coronary artery ligation. In each group food and fluid as well as sodium intake, urine (Vu), sodium (UNaV), potassium (UKV) and solutes (UosmV) excretion were determined before and four weeks after the surgery. Size of the infarct, left ventricle (LV) weight and diameter of LV and right ventricle (RV) myocytes were determined during post-mortem examination. Before the surgery groups 3 and 4 ingested significantly more fluid and sodium, had higher Vu, UNaV, UKV and UosmV than the respective groups 1 and 2. In groups 2 and 4 MI resulted in significant decrease in Vu, UNaV and UosmV in comparison to the pre-surgical level. In Group 4 MI resulted also in a significant decrease of food and sodium intake. The MI size did not differ in groups 2 and 4 while diameter of LV myocytes was significantly greater in groups 2 and 4 than in groups 1 and 3, and in group 4 than in group 2. The study reveals that prolonged high sodium consumption increases fluid and electrolyte turnover both in the sham and in the MI rats and that the MI causes decrease in food and sodium intake in rats on high but not on regular sodium intake. In addition high sodium diet promotes development of greater post-MI hypertrophy of the LV myocytes.
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