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1

Izoprenylacja bialek

100%

Jamroz-Wisniewska A., Beltowski J.

Postępy Biochemii

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2004

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tom 50

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nr 4

316-329

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Sectrophotometric assay of renal ouabain-resistant Naplus-ATPase and its regulation by leptin and dietary-induced obesity

80%

Beltowski J., Jamroz-Wisniewska A., Nazar J., Wojcicka G.

Acta Biochimica Polonica

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2004

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tom 51

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nr 4

Apart from Na,K-ATPase, a second sodium pump, Na-stimulated, ^-independent ATPase (Na -ATPase) is expressed in proximal convoluted tubule of the mammalian kidney. The aim of this study was to develop a method of Na -ATPase assay based on the method previously used by us to measure Na ,K -ATPase activity (Acta Biochim Polon.; 2002, 49: 515-27). The ATPase activity was assayed as the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Na -ATPase activity was calculated as the difference between the activities measured in the presence and in the absence of 50 mM NaCl. Na -ATPase activity was detected in the renal cortex (3.5 ± 0.2 ^mol phosphate/h per mg protein), but not in the renal medulla. Na -ATPase was not inhibited by ouabain or an H ,K -ATPase inhibitor, Sch 28080, but was almost completely blocked by 2 mM furosemide. Leptin administered intraperitoneally (1 mg/kg) decreased the Na ,K -ATPase activity in the renal medulla at 0.5 and 1 h by 22.1% and 27.1%, respectively, but had no effect on Na -ATPase in the renal cortex. Chronic hyperleptinemia induced by repeated subcutaneous leptin injections (0.25 mg/kg twice daily for 7 days) increased cortical Na,K-ATPase, medullary Na,K-ATPase and cortical Na+-ATPase by 32.4%, 84.2% and 62.9%, respectively. In rats with dietary-induced obesity, the Na ,K - ATPase activity was higher in the renal cortex and medulla by 19.7% and 34.3%, respectively, but Na -ATPase was not different from control. These data indicate that both renal Na -dependent ATPases are separately regulated and that up-regulation of Na -ATPase may contribute to Na retention and arterial hypertension induced by chronic hyperleptinemia.

3

Nitric oxide - superoxide cooperation in the regulation of renal Naplus, Kplus -ATPase

80%

Beltowski J., Marciniak A., Jamroz-Wisniewska A., Borkowska E.

Acta Biochimica Polonica

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2004

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tom 51

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nr 4

The aim of this study was to investigate whether endogenous superoxide anion is involved in the regulation of renal Na+ ,K+ -ATPase and ouabain-sensitive H+,K+-ATPase activities. The study was performed in male Wistar rats. Compounds modulating superoxide anion concentration were infused under general anaesthesia into the abdominal aorta proximally to the renal arteries. The activity of ATPases was assayed in isolated microsomal fraction. We found that infusion of a superoxide anion-generating mixture, xanthine oxidase (1 mU/min per kg) + hypoxanthine (0.2 umol/min per kg), increased the medullary Na+ ,K+ -ATPase activity by 49.5% but had no effect on cortical Na+ ,K+ -ATPase and either cortical or medullary ouabain-sensitive H+ ,K+ -ATPase. This effect was reproduced by elevating endogenous superoxide anion with a superoxide dismutase inhibitor, diethylthiocarbamate. In contrast, a superoxide dismutase mimetic, TEMPOL, decreased the medullary Na+ ,K+ -ATPase activity. The inhibitory effect of TEMPOL was abolished by inhibitors of nitric oxide synthase (l-NAME), soluble guanylate cyclase (ODQ) and protein kinase G (KT5823). The stimulatory effect of diethylthiocarbamate was not observed in animals pretreated with a synthetic cGMP analogue, 8-bromo-cGMP. An inhibitor of NAD(P)H oxidase, apocynin (1 ^mol/min per kg), decreased the Na+ ,K+ -ATPase activity in the renal medulla and its effect was prevented by L-NAME, ODQ or KT5823. In contrast, a xanthine oxidase inhibitor, oxypurinol, administered at the same dose was without effect. These data suggest that NAD(P)H oxidase-derived superoxide anion increases Na+,K+-ATPase activity in the renal medulla by reducing the availability of NO. Excessive intrarenal generation of superoxide anion may upregulate medullary Na+,K+-ATPase leading to sodium retention and blood pressure elevation.

4

Time-dependent effect of leptin on renal Naplus, Kplus-ATPase activity

80%

Marciniak A., Jamroz-Wisniewska A., Borkowska E., Beltowski J.

Acta Biochimica Polonica

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2005

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tom 52

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nr 4

Leptin, secreted by adipose tissue, is involved in the pathogenesis of arterial hypertension, however, the mechanisms through which leptin increases blood pressure are incompletely elucidated. We investigated the effect of leptin, administered for different time periods, on renal Na+,K+-ATPase activity in the rat. Leptin was infused under anesthesia into the abdominal aorta proximally to the renal arteries for 0.5-3 h. Leptin administered at doses of 1 and 10 μg/min per kg for 30 min decreased the Na+,K+-ATPase activity in the renal medulla. This effect disappeared when the hormone was infused for ≥1 h. Leptin infused for 3 h increased the Na+,K+-ATPase activity in the renal cortex and medulla. The stimulatory effect was abolished by a specific inhibitor of Janus kinases (JAKs), tyrphostin AG490, as well as by an NAD(P)H oxidase inhibitor, apocynin. Leptin increased urinary excretion of hydrogen peroxide (H2O2) between 2 and 3 h of infusion. The effect of leptin on renal Na+,K+-ATPase and urinary H2O2 was augmented by a superoxide dismutase mimetic, tempol, and was abolished by catalase. In addition, infusion of H2O2 for 30 min increased the Na+,K+-ATPase activity. Inhibitors of extracellular signal regulated kinases (ERKs), PD98059 or U0126, prevented Na+,K+-ATPase stimulation by leptin and H2O2. These data indicate that leptin, by acting directly within the kidney, has a delayed stimulatory effect on Na+,K+-ATPase, mediated by JAKs, H2O2 and ERKs. This mechanism may contribute to the abnormal renal Na+ handling in diseases associated with chronic hyperleptinemia such as diabetes and obesity.

5

Bidirectional regulation of renal cortical Naplus, Kplus-ATPase by protein kinase C

71%

Beltowski J., Marciniak A., Jamroz-Wisniewska A., Borkowska E., Wojcicka G.

Acta Biochimica Polonica

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2004

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tom 51

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nr 3

We examined the role of protein kinase C (PKC) in the regulation of Na+,K+- ATPase activity in the renal cortex. Male Wistar rats were anaesthetized and the investigated reagents were infused into the abdominal aorta proximally to the renal arteries. A PKC-activating phorbol ester, phorbol 12,13-dibutyrate (PDBu), had a dose-dependent effect on cortical Na+ ,K+ -ATPase activity. Low dose of PDBu (10- mol/kg per min) increased cortical Na+ ,K+ -ATPase activity by 34.2%, whereas high doses (10-9 and 10-8 mol/kg per min) reduced this activity by 22.7% and 35.0%, respectively. PDBu administration caused changes in Na+ ,K+ -ATPase Vmax without affecting K0.5 for Na+ , K+ and ATP as well as K for ouabain. The effects of PDBu were abolished by PKC inhibitors, staurosporine, GF109203X, and Go 6976. The inhibitory effect of PDBu was reversed by pretreatment with inhibitors of cytochrome P450-dependent arachidonate metabolism, ethoxyresorufin and 17-octadecynoic acid, inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY294002, and by actin depolymerizing agents, cytochalasin D and latrunculin B. These results suggest that PKC may either stimulate or inhibit renal cortical Na+ ,K+ -ATPase. The inhibitory effect is mediated by cytochrome P450-dependent arachidonate metabolites and PI3K, and is caused by redistribution of the sodium pump from the plasma membrane to the inactive intracellular pool.

6

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Subdural haematoma mimicking empyema in a patient with multiple sclerosis treated with immunosuppressive monoclonal antibody

61%

Ciesielska M., Jamroz-Wisniewska A., Bak M., Chmielewska P., Nowakowska M., Rejdak K.

Journal of Pre-Clinical and Clinical Research

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2018

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tom 12

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nr 4

7

Progressive forms of multiple sclerosis: disease-modifying therapy review

61%

Sapko K., Szczepanska-Szerej A., Jamroz-Wisniewska A., Kulczynski M., Marciniec M., Rejdak K.

World Scientific News

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2018

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tom 105

8

Successful surgical treatment in a patient with a giant pituitary macroadenoma accompanied by obstructive hydrocephalus

61%

Rawska A., Salek M., Nowakowska M., Bak M., Jamroz-Wisniewska A., Rejdak K.

Journal of Pre-Clinical and Clinical Research

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2019

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tom 13

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nr 3

9

Rare cause of rapidly progressive dementia – Creutzfeldt-Jakob disease (CJD) with negative 14-3-3 protein – Case Report

61%

Bak M., Jamroz-Wisniewska A., Nowakowska M., Ciesielka M., Salek M., Rawska A., Rejdak K.

Journal of Pre-Clinical and Clinical Research

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2019

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tom 13

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nr 3

10

Susac syndrome as a multidisciplinary diagnostic challenge

51%

Sapko K., Jamroz-Wisniewska A., Wozniak A., Marciniec M., Kulczynski M., Janczarek M., Rejdak R., Rejdak K.

Annals of Agricultural and Environmental Medicine

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2022

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tom 29

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nr 1

Ograniczanie wyników

Izoprenylacja bialek

Sectrophotometric assay of renal ouabain-resistant Naplus-ATPase and its regulation by leptin and dietary-induced obesity

Nitric oxide - superoxide cooperation in the regulation of renal Naplus, Kplus -ATPase

Time-dependent effect of leptin on renal Naplus, Kplus-ATPase activity

Bidirectional regulation of renal cortical Naplus, Kplus-ATPase by protein kinase C

Subdural haematoma mimicking empyema in a patient with multiple sclerosis treated with immunosuppressive monoclonal antibody

Progressive forms of multiple sclerosis: disease-modifying therapy review

Successful surgical treatment in a patient with a giant pituitary macroadenoma accompanied by obstructive hydrocephalus

Rare cause of rapidly progressive dementia – Creutzfeldt-Jakob disease (CJD) with negative 14-3-3 protein – Case Report

Susac syndrome as a multidisciplinary diagnostic challenge