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Changes of Ca2+/calmodulin - dependent protein kinase-II after transient ischemia in gerbil hippocampus

100%
Zalewska T., Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
41-48
EN
Transient cerebral ischemia induces, besides delayed neurodegeneration in selected brain structures, a number of early responses which may mediate ischemic injury/repair processes. Here we report that 5 min exposure to cerebral ischemia in gerbils induces a rapid inhibition and subsequent translocation of Ca (2+)/calmodulin-dependent protein kinase II (CaMKII). These changes were partially reversible during a 24 h post-ischemic recovery. Concomitantly the total amount of the enzyme protein, as revealed by Western blotting (alfa- -subunit specific), remained stable. This is consistent with our previous hypothesis, that the mechanism of ischemic CaMKII down-regulation involves a reversible posttranslational modification-(auto)phosphorylation, rather then the degradation of enzyme protein. The effectiveness of known modulators of postischemic outcome in counteracting CaMKII inhibition was tested. Three of these drugs, namely dizocilpine (MK-801), N-nitro-L-arginine methyl ester (L-NAME) and gingkolide (BN52021), all significantly attenuated the enzyme response to ischemia, whereas an obvious diversity in the time-course of their actions implicates different mechanisms involved.
2
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Protein serine/threonine kinases (PKA, PKC and CaMKII) involved in ischemic brain pathology

100%
Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
579-585
EN
The protein serina/threonine kinases which are highly expressed in the central nervous system (CNS) are severely affected by brain ischemia.Irrespective of substantial differences among the particular members of this group of kinases, their responses to ischemic stress show a lot of similarities.Initially they are switched on fy faciliated interaction with their specific activators/second messengers like cyclic AMP, 1,2 -sn-diacylglicrol and particularly Ca2+, then they are translocated to highly specific regions of plasma membranes.After phosphorylation of target proteins, the kinases are deactivated by means access to cAMP. In the case of CaMKII, it is probably achieved by its extensive, inhibitory autophosphorylations, while PKC seems to be proteolytically degraded.These biphasic changes in serine/threonine kinases activity may play a critical role in the evolution of postichemic brain injury and provide a mechanism for a variety of short- and long-term signalling events.
3
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Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

80%
Strosznajder J., Chalimoniuk M.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
71-81
EN
This study was aimed to examine properties and changes in nitric oxide synthase (NOS) activity and cGMP level during reperfusion after 5 min of brain ischemia in gerbils. Animals were treated 5 min befor ischemia with NOS inhibitors: N-nitro-L-arginine (NNLA), or 7-Nitroindazole (7-NI), or with the inhibitor of guanylate cyclase, LY 83583, or with hydrocortisone for 7 days before ischemia. Northern bolt analysis was performed using specific cDNA for inducible NOS. It was observed that ischemia significantly enhances NOS activity and cGMP level. During reperfusion, biphasic increase in NOS activity and cGMP level took place with two peaks 15 min and 2 h after ischemia. NNLA, 7-NI, and LY 83583 eliminated enhancements of NOS activity and cGMP level, whereas glucocorticoid remained without effect. There was no activation of gene encoding inducible NOS (iNOS). Our results indicate that ischemia-reperfusion activates constitutive NOS. It is suggested that nitric oxide (NO) production during reperfusion is related to neuronal degeneration and that inhibitor of NOS offers a new therapeutical strategies.
4
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Interrelations between nuclear-factor kappa B activation, glial response and neuronal apoptosis in gerbil hippocampus after ischemia

61%
Domanska-Janik K., Bronisz-Kowalczyk A., Zajac H., Zablocka B.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 1
45-51
EN
Spatial and temporal relations between transcriptional factor NFkB activation and glia reaction in gerbil hippocampus after transient cerebral ischemia has been studied. Activation of protein binding to NFkB consensus oligonucleotide was determined by electrophoretic mobility gel shift assay (EMSA) in homogenates from dorsal (DP- an equivalent of CA1 sector) and abdominal (AbP- containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of NFkB binding was observed exclusively in DP as early as 3 h after ischemia and at this time that response preceded any other morphological signs of postischemic tissue injury. This early enhancement of NFkB binding was followed by microglia activation visualized in CA1 pyramidal region at 24 h of recovery by histochemical staining with lectin from Ricinus communis (RCA-120). Simultaneously, only a moderate increase of immunostaining against glial fibrillary acidic protein (GFAP) was observed homogeneously in all parts of hippocampus. This uniform pattern of astrogliosis was preserved until postischemic day 3-4, when apoptotic DNA fragmentation in CA1 pyramidal neurons had been clearly documented by TUNEL staining. At this period however, continuous elevation of NFkB binding in DP corresponded with similar response manifested also in AbP of the hippocampus. These results evidence a preferential NFkB involvement in an early microglia activation in the apoptogenic CA1 sector, although its role in a later astrocytic response to ischemia could not be neglected too.
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