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1

Ogólnopolska konferencja użytkowników oprogramowania statystycznego R

100%
Beresewicz M.
Wiadomości Statystyczne
|
2015
|
tom 60
|
nr 01
2

Bialka kotwiczace i ich udzial w przekazywaniu sygnalow w zageszczeniu postsynaptycznym w osrodkowym ukladzie nerwowym

100%
Beresewicz M.
Postępy Biochemii
|
2007
|
tom 53
|
nr 2
188-197
3

SI-01 balance between JNK and MAP kinase cascades activation in hippocampus in norm and in ischemic pathology

71%
Beresewicz M., Beresewicz M., Kowalczyk J. E., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
4

Impaired balance between JNK and MAP kinase cascades activation in postsynaptic density after transient brain ischemia

63%
Beresewicz M., Zablocka B.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
5
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Estymacja liczby cudzoziemców w Polsce z wykorzystaniem metody capture-recapture

51%
Beresewicz M., Gudaszewski G., Szymkowiak M.
Wiadomości Statystyczne
|
2019
|
tom 64
|
nr 10
6

PKC delta and beta translocation to mitochondria correlates with opposite susceptibility of hippocampal regions to ischemic insult

51%
Kowalczyk E., Beresewicz M., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
7

Role of mitochondria in the delayed neuronal death after transient brain ischemia n vivo

51%
Kowalczyk J. E., Beresewicz M., Zablocka B.
Acta Biochimica Polonica
|
2006
|
tom 53
|
nr Supplement 1
8

Diazepam and cyclosporin A:the promising neuroprotectants

51%
Sarnowska A., Beresewicz M., Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
9

Upregulation of IGF-1B (MGF) in neonatal stroke

45%
Majewska M., Beresewicz M., Makarewicz D., Gorecki D. C., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
10

A novel voltage-gated potassium channel in hippocampal mitochondria

39%
Kowalczyk J. E., Bednarczyk P., Beresewicz M., Dolowy K., Szewczyk A., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Transient cerebral ischemia is known to induce endogenous adaptive mechanisms such as the activation of mitochondrial ATP-sensitive potassium channels or calcium-sensitive largeconductance potassium channels that can prevent or delay neuronal injury. In this study a single channel activity was measured after patch-clamp of the mitoplasts isolated from control gerbil hippocampus. In 70% of the all patches, a potassium selective current was recorded with mean conductance 109 ± 6 pS in symmetrical 150 mM KCl solution. Patch-clamp single channel studies protein showed properties of the voltage-gated potassium channel (Kv channel): it was blocked by negative voltage and margatoxin (MgTx) a specifi c Kv1.3 inhibitor. The inhibition by MgTx was no reversed. The channel was not affected by the other Kv1.3 channel blocker agitoxin-2 at nanomolar range. Additionally, we showed that ATP/Mg2+ complex and low or high concentration of Ca2+ ions have no effects on observed activity of ion channel. Mitochondrial localization of Kv1.3 was verifi ed by western blots using antibodies recognizing peptides located in N- or C-terminal of plasma membrane Kv1.3 protein. N-terminal specifi c antibodies recognized proteins with molecular masses around 95, 62 and 40 kDa in plasma membrane and 60 kDa in mitochondria while C-terminal specifi c antibodies recognized 40 kDa protein in mitochondria. Mitochondrial localization of Kv1.3 protein was also shown by immunohistochemistry. We conclude that gerbil hippocampus mitochondria contain voltagegated potassium channel (mitoKv) with properties similar to the surface membrane Kv1.3 channel which can play an important regulatory role for protection with respect of ischemia-reperfusion phenomena. Supported by Polish Mitochondrial Network MitoNet.pl
11

A link between glutamine metabolism and selective neuronal vulnerability in the hippocampus

39%
Bochomulski P., Krupska O., Klimczak P., Hilgier W., Zablocka B., Beresewicz M.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: The brain has developed several endogenous mechanisms to protect itself from the harm ful consequences of ischemia/reperfusion (I/R) injury. Understanding of such mechanisms may be important for the development of new neuroprotective therapies. In a gerbil model of cerebral ischemia, 5 min-ischemia results in selective, delayed neuronal death in the hippocampal CA1 region, while CA2‑4 and the DG remains relatively resistant. We have shown that I/R‑induced translocation of protein kinase C beta II (PKCβII) from cytoplasm to mitochondria only in CA2‑4 and the DG is relevant for ischemia‑resistance of these regions. The exact mechanism remains unknown. AIM(S): The aim of the study was to investigate the role of kidney‑type glutaminase (GLS1), identified as a potential PKCβII partner, in PKCβII‑mediated neuroprotection. METHOD(S): Reciprocal co-immunoprecipitation method showed that of the two GLS1 isoforms, it is GAC not KGA that interacts with PKCβII. In vitro studies revealed that GLS1 may be phosphorylated by PKCβII. GLS1 converts glutamine to glutamate, thus the effect of I/R on activity of GLS1 and level of glutamine and glutamate in mitochondria-enriched fraction were measured. RESULTS: Glutaminase activity is higher in CA2‑4 and DG as compared to CA1 in control and 1 h after I/R, and is confirmed by a reduced level of glutamine in this region. Glutamate level seems to be similar in both regions and is not affected by I/R injury. Application of a selective PKCβII inhibitor increased GLS1 activity in both regions. CONCLUSIONS: This indicates that GAC is not relevant in PKCβII‑mediated neuroprotection, however PKCβII seems to have an influence on the maintenance of glutaminase activity. Moreover, we speculate that ischemia‑resistance of CA2‑4 and the DG is due to its high glutaminase activity, which provides a large amount of glutamate that, in turn, can be effectively used for ATP production in the Krebs cycle or for antioxidant defense based on glutathione synthesis. FINANCIAL SUPPORT: This work was supported by National Science Centre grant 2014/15/D/NZ3/02784.
12

Voltage-gated potassium channel in hippocampus mitochondria

39%
Bednarczyk P., Kowalczyk J. E., Beresewicz M., Dolowy K., Szewczyk A., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Transient cerebral ischemia is known to induce endogenous adaptive mechanisms such as the activation of mitochondrial ATP regulated or Ca2+ regulated large conductance potassium channels that can prevent or delay neuronal injury. However, molecular mechanism of this effect remains unclear. In this study, a single channel activity was measured with patch-clamp of the mitoplasts isolated from gerbil hippocampus. In 70% of the all patches, a potassium selective current with properties of the voltage-gated potassium channel (Kv type channel) was recorded with mean conductance 109 ± 6 pS in symmetrical 150 mM KCl solution. Detected channel was blocked by negative voltage and margatoxin (MgTx) a specific Kv1.3 channel inhibitor. The inhibition by MgTx was irreversible. We observed that ATP/Mg2+ complex or Ca2+ ions had no effects on observed activity of ion channel. Additionally, we showed that agitoxin-2 (AgTx-2), potent inhibitor of the voltage-gated potassium channels, was without effect on channel activity. This observation suggests that mitochondrial voltage-gated potassium channel can represent different molecular structure without affinity to AgTx-2 in compare to surface membrane channels. Also, Western blot analysis of mitochondria isolated from gerbil hippocampus and immunohistochemistry on gerbil brain sections confirm the expression of Kv1.3 protein in mitochondria. All together, we conclude that gerbil hippocampal mitochondria contain voltage-gated potassium channel (mitoKv1.3 channel) with properties similar to the surface membrane Kv1.3 channel which can influence function of mitochondria in physiological and pathological conditions. This study was supported by the grant from the Ministry of Science and Higher Education (P-N/31/2006) and Polish Mitochondrial Network MitoNet.pl. P.B. would like to acknowledge to prof. Detlef Siemen for teaching patch-clamp and more discussion during postdoc in Magdeburg supported by EMBO (2006) and DAAD (2008).
13

Role of the blood - brain barrier in differential response to opioid peptides and morphine in mouse lines divergently bred for high and low swim stress - induced analgesia

33%
Kosson A., Krizbai I., Lesniak A., Beresewicz M., Sacharczuk M., Kosson P., Nagyoszi P., Wilhelm I., Kleczkowska P., Lipkowski A. W.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 1
Over 20 years ago, the Sadowski group separated two mouse lines, one with high (HA) and the other with low (LA) sensitivity to swim stress-induced analgesia (SSIA). Recently, we proposed that increased leakage of the blood-brain barrier (BBB) in the HA line created the difference in the response to SSIA. To search for further evidence for this hypothesis, differences in the levels of the BBB proteins occludin and claudin-5 were analysed. In addition, we sought to evaluate practical differences in BBB permeability by examining the antinociceptive levels in HA and LA mouse lines after i.v. administration of peptides that have limited access to the CNS. Western blot was used to analyse the differences between occludin and claudin-5. To evaluate the functional differences between the BBB of HA and LA mice, the antinociception levels of endomorphin I, biphalin and AA2016 (peptides with limited BBB permeabilities) in the tail flick test were examined. The expression levels of occludin and claudin-5 in the HA mouse line were lower than in the LA and control mice. Central antinociception of the opioid peptides were significantly higher in the HA line than in the LA and control lines. Our data support the hypothesis that BBB leakage is responsible for the differences between the HA and LA mouse lines. Although SSIA confirmed BBB differences between both lines, it is not limited to the opioid system and could be a useful model for studying the role of the BBB in molecular communications between the periphery and CNS.
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