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1

Metaloproteazy w fizjologii i patologii osrodkowego ukladu nerwowego

100%
Ziemka-Nalecz M.
Postępy Biologii Komórki
|
2003
|
tom 30
|
nr 4
721-734
2

Neuroprotective effects of histone deacetylase inhibitors in brain ischemia

63%
Ziemka-Nalecz M., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 4
Stroke resulting from cerebral ischemia or haemorrhage is a common cause of the death of neuronal cells and neurological dysfunction in humans. Finding therapeutics to improve outcome from brain ischemic injury has proved to be challenging. The efficacy of neuroprotective compounds identified in experimental brain ischemia models thus far have failed to successfully translate in clinical human trials. Recent experimental evidence indicates that inhibition of zinc-dependent histone deacetylases can protect neuronal and oligodendroglial cells from the damaging effects of ischemic insult, which may contribute to improved functional outcome. In this review we briefly highlight the current data supporting a beneficial role of histone deacetylation in experimental brain ischemia. We also discuss the molecular mechanism of neuroprotection.
3

Endogenous neurogenesis induced by ischemic brain injury or neurodegenerative diseases in adults

63%
Ziemka-Nalecz M., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2012
|
tom 72
|
nr 4
The discovery of neurogenic response subsequent to brain injuries has led to the hypothesis that the expansion of the pool of endogenous progenitors could augment the regenerative capacity of the damaged areas. However, it occurred that endogenous spontaneous neurogenesis is insufficient for replacing the lost neurons and to achieve global repair, particularly in aging brain. Until today, a great effort has been made attempting to promote "reactive neurogenesis" more successful. It was found that small chemical molecules exert stimulation of neurogenesis and probably might help to induce neuronal endogenous cell replacement in various neurological diseases. In this review we briefly highlight the current data regarding effect of brain ischemia and age-related neurodegenerative diseases on neural stem cells in situ and potential therapeutic effect of their stimulation.
4

Oxygen-glucose deprivation promotes gliogenesis and micrologia activation in organotypic hippocampal slice culture: Involvement of metalloproteinases

51%
Ziemka-Nalecz M., Stanaszek L., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Brain ischemia resembles other brain injuries in producing enhanced neurogenesis in neuroproliferative regions of the rodent brain, including subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus (DG) of the hippocampus. Newly-generated neurons would be incorporated in the hippocampal local circuitry and involved in brain repair. Organotypic culture of hippocampal slices (OHC) provides an alternative model of hippocampus in vivo. Moreover, exposure of the organotypic slices to oxygen and glucose deprivation (OGD) mimics cerebral ischemia. The aim of the present study was to investigate whether deprivation of oxygen and glucose might stimulate cell proliferation and neurogenesis in organotypic hippocampal slice culture. Furthermore, we evaluate whether the activity of matrix metalloproteinases (MMPs) in the OHC parallels the rate of cell proliferation and/or further differentiation. Cell death in the organotypic hippocampal slices was determined with propidium iodide (IP) staining. Stem cells proliferation was detected by using DNA replication marker – 5-Bromo 2-Deoxyuridine (BrdU) followed by immunoreaction with specific antibodies. Newly generated BrdU(+) cells were identified by an analysis of neural, glial and microglial markers expression – NF-200 NeuN, GFAP, ED1, respectively. In order to check the activity and localization of metalloproteinases, MMP-2 and MMP-9, we conducted in situ zymography in conjunction with immunohistochemistry. Exposing rat OHC for 40 min OGD followed by 24h of reoxygenation induces cell death in CA1 area with only negligible damage in DG. At 1 week cell death appears all over the slice in control conditions as well as after OGD. The stimulation of cell proliferation was observed 7 days after OGD exclusively in CA1. At the same time the number of BrdU(+) cells in DG remained on the level characteristic for control cultures. The majority of BrdU positive cells presents expression of microglial specific stain (ED1) pronounced particularly in CA1 at 3 days after OGD. However, some BrdU labeled nuclei were encapsulated by GFAP positive processes especially in CA1 region of the hippocampus (3 and 7 days after OGD). We do not notice coexpression of BrdU-positive cells with NeuN(+) mature neurons. The study suggests that slice cultures do not show neurogenesis for chosen cultivation period. Activation of MMPs was localized mainly in microglial cells and may be associated with their proliferation in situ. Supported by MSHE grant no 0154/B/P01/2010/38
5

Correlation between activity of metalloproteinases and apoptosis in rat primary cortical cultute-the effect of CsA and FK-506

51%
Berdowska P., Ziemka-Nalecz M., Buzanska L., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
6

Oxygen-glucose deprivation (OGD) promotes microglia activation and gliogenesis but not neurogenesis in organotypic hippocampal slice culture (OHC)

51%
Ziemka-Nalecz M., Wojcik-Stanaszek L., Zajac H., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Organotypic hippocampal cultures are used as an alternative model for studying molecular mechanism(s) of neurogenesis after combined oxygen-glucose deprivation (OGD) mimicking ischemic conditions. The aim of the present work was to investigate the effect of OGD on stem/progenitor cells proliferation and/or differentiation in the hippocampus. Our attention was primarily focused on the relationship between neurogenesis-associated processes and activity of matrix metalloproteinases (MMPs). Cell proliferation was detected by using BrdU incorporation. Newly generated BrdU (+) cells were identified by labeling with specific cell markers. In order to check the activity and localization of MMPs we conducted in situ zymography in conjunction with immunohistochemistry. In our experimental conditions OGD-insult followed by 24 h of recovery caused the damage of neuronal cells in CA1. At 1 week cell death appears all over the hippocampus. We found that expected stimulation of endogenous neurogenesis fails as a source of compensation for the lost neurons in OGD-treated cultures. The modulation of culture microenvironment after ischemia favors the dominant proliferation of glial cells expressed by the enhancement of newly-generated oligodendrocyte progenitors. In addition, during our study we also detected some BrdU labeled nuclei encapsulated by GFAP positive processes. However, the majority of BrdU positive cells expressed microglial specific stain, particularly pronounced in CAlarea. The OGD-promoted responses involved activation of metalloproteinases, which matches the progression of gliogenesis. On the other hand, the high activity of MMPs associated with microglial cells implicate their involvement in the mechanism participating in OGD-induced cell damage.
7

The potential role of FAK- and PYK2 coupled pathway in the neurogenesis in gerbil hippocampus after global ischemia

51%
Ziemka-Nalecz M., Wojcik-Stanaszek L., Zajac H., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Recently published data indicate that in physiological conditions proteolytic remodeling of extracellular matrix (ECM) by matrix metalloproteinases (MMPs) participates in the stem cells development. Signal derived from ECM may activate specific intracellular signaling pathways which involve non-receptor tyrosine kinases such focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), key components responsible for the flow of information to the cell. FAK and Pyk2 might act through a diverse array of downstream molecules such a phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK). Activation (PI3K)/ Akt and ERK pathways in neural precursors plays a central role in induction of adult neurogenesis. These prompted us to evaluate the possible involvement of FAK/PYK2-coupled pathway in the regulation of neurogenesis-associated processes stimulated by transient global ischemia in gerbil hippocampus. For this purpose we checked if there is temporal relationship between activation/phosphorylation of these kinases and proliferation and/or determination of neural progenitor cells. We found that short-term (5 min) ischemia increased Pyk-2 phosphorylation level in dentate gyrus ( neurogenic part of hippocampus) after 2 and 4 weeks of recovery, the time when we observed the intensive proliferation rate and differentiation of progenitors toward neuronal phenotypes. In contrast, in the CA1 region of the hippocampus the level of phosphorylated Pyk-2 was slightly reduced after 2, 4 and 6 weeks of reperfusion. At the same time the level of phosphorylated FAK was significantly increased in both investigated hippocampal regions. In contrast activation of ERK and Akt kinases was significantly reduced in all investigated time points with more pronounced effect in CA1. The elevation of PYK-2 activity in dentate gyrus might suggest the involvement of this kinase in the post-ischemic stimulation of neurogenesis after global ischemia.
8

Neonatal cerebral hypoxia-ischemia:involvement of FAK-dependent pathway

51%
Ziemka-Nalecz M., Makarewicz D., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
9

FAK-and Pyk2-coupled pathway may contribute to the neurogenesis in gerbil hippocampus after ischemia

51%
Ziemka-Nalecz M., Wojcik-Stanaszek L., Zajac H., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Recently published data indicate that in physiological conditions proteolytic remodeling of extracellular matrix (ECM) by matrix metalloproteinases (MMPs) participates in the stem cells development. Signal derived from ECM may activate specific intracellular signaling pathways which involve non-receptor tyrosine kinases such focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), key components responsible for their flow of information to the cell. The function of these enzymes is believed to be tightly linked to its autophosphorylation and association with Src kinase necessary for reciprocal activation/phosphorylation of both enzymes in response to adhesion-dependent signals. FAK and Pyk2 might act through a diverse array of downstream molecules and may regulate biological functions of the cell. These prompted us to evaluate the possible involvement of FAK/PYK2-coupled pathway in the regulation of neurogenesis-associated processes stimulated by transient global ischemia in gerbil hippocampus. For this purpose we checked if there is temporal relationship between activation/phosphorylation of both kinases and proliferation and/or determination of neural progenitor cells. We found that short-term (5 min) ischemia increased Pyk-2 phosphorylation level in dentate gyrus ( neurogenic part of hippocampus) after 2 and 4 weeks of recovery, the time when we observed the intensive proliferation rate and differentiation of progenitors toward neuronal phenotypes. In contrast, in the CA1 region of the hippocampus the level of phosphorylated Pyk-2 was slightly reduced after 2, 4 and 6 weeks of reperfusion. At the same time the level of phosphorylated FAK was significantly increased in both investigated hippocampal regions. The elevation of PYK-2 activity in dentate gyrus might suggest the involvement of this kinase in the post-ischemic stimulation of neurogenesis after global ischemia. Supported by MSHE grant no 0154/B/P01/2009/38.
10

Involvement of MMPs in delayed neuronal death after global ischemia

51%
Zalewska T., Ziemka-Nalecz M., Sarnowska A., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
|
2002
|
tom 62
|
nr 2
11

New model of experimental stroke in rats:cellular networking in response to injury

45%
Kozlowska H., Janowski M., Ziemka-Nalecz M., Wanacka E., Lukomska B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
12

Potential role of MMP-2 and-9 in ischemia-stimulated neurogenesis in the gerbil hippocampus

45%
Wojcik-Stanaszek L., Szymczak P., Ziemka-Nalecz M., Zajac H., Zalewska T.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Matrix metalloproteinases (MMPs) are a growing family of zincdependent endopeptidases that are classically recognized as matrixremodeling enzymes implicated in various physiological and pathological processes. Apart from relatively well established detrimental role of MMPs, in particular gelatinases (MMP-2 and MMP-9), following brain injury, MMPs have been considered recently to be involved in the neurogenic response of the adult neural stem/progenitor cells after ischemic challenge. However, the role of these enzymes in the neurogenesis still remains to be clarified. The goal of the present study was to elucidate if activation of MMPs parallels the rate of neural progenitor cells proliferation and/or further differentiation. Our results show that post-ischemic acceleration in the proliferation and differentiation of progenitors in the dentate gyrus of the adult hippocampus coincides with the remarkable elevation of MMPs activity. On the contrary, in the ischemia-damaged CA1 pyramidal cells layer the activity of MMPs fell below the control level. It should be pointed out, that in this structure neurogenesis seems to be rather elusive, as we did not found evidence for production of a new matured neurons. In an effort to further check the potential participation of MMPs in neurogenesis-associated processes we have tested the effect of MMPs inhibitors (GM6001 and doxycycline) on neural stem cells line. We observed that the addition of these agents decreased the rate of proliferation and differentiation toward neurons. In conclusion, the spatial and temporal profile of MMPs activity during reperfusion following transient forebrain ischemia suggest that these proteinases might belong to the discussed mechanism(s) which govern neurogenesis-associated processes in ischemic brain hippocampus. Supported by MSHE grant no 0154/B/P01/2009/38.
13
Content available remote

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

39%
Dragun P., Makarewicz D., Wojcik L., Ziemka-Nalecz M., Slomka M., Zalewska T.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 3
441-455
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and carry out key functions during brain development. Apart from a physiological role, excessive activation of MMPs in brain tissue has been postulated to represent a pathway for cell death arising from ischemia. To evaluate the possible involvement of MMPs in the perinatal brain asphyxia, we exposed 7-day-old rats to hypoxia-ischemia (HI). Unilateral HI was administered by ligation of the common carotid artery followed by hypoxia (7.4% O2/92.6% N2) for 65 minutes. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in > 90% of animals. HI resulted in a significant elevation of MMP-2 and MMP-9 activity in the ipsilateral forebrain. The maximum activation was found at 48 hours and 7-14 days after the insult. These results suggest that early and late induction of MMPs may play a role in neuronal death as well as in repair processes. The treatment of animals subjected to HI with 1-methylnicotinamide (MNA), the anti-inflammatory agent, led to the inhibition of MMP-9 in an acute phase of ischemic damage and to the activation of MMP-2 in the later stages after injury. The timing of MMPs modulation by MNA may indicate its possible therapeutic implications.
14

The modulation of HIFs, pluripotency and differentiation genes expression by oxygen conditions in neural stem cells derived from human cord blood

39%
Szablowska-Gadomska I., Drela K., Podobinska M., Ziemka-Nalecz M., Domanska-Janik K., Buzanska L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
The oxygen tension is an important factor modulating cell fate and developmental decisions. There are evidences that HIFs (Hypoxia Inducible Factors) family is implicated in the regulation of pluripotency and differentiation genes. The goal of this study is to compare the influence of close to physiological oxygen conditions (5%) to atmospheric oxygen tension on differentiation process and pluripotent activity in HUCB-NSC. The expression of Hypoxia Inducible Factors, stemness and neural differentiation markers in NSC, cultured under 5% and 21% oxygen were checked on the transcriptional and translational level. We were looking at the interaction between HIFs (HIF1 alpha, HIF 2 alpha) and activity of neural differentiations genes (MAP2, GFAP, β-tubulin) as well as expression of pluripotency genes (Oct4, Sox2, Rex1 and Nanog). In order to demonstrate the impact of increased HIF1α and/ or HIF2α level on cell differentiation we used DMOG (Sigma) which is of prolyl-4-hydroksylase inhibitor to increase HIF alpha levels. Our data show, that low oxygen conditions promote proliferation of HUCBNSC at early stage of development and can activate Oct4 and Nanog genes in HUCB-NSC. The time of cultivation of the cells in low oxygen conditions and the developmental stage of the cells are the important factors for the induction of the expression of “pluripotency” genes.Hypoxia Inducible Factors HIF 1α and HIF 2α, but not HIF3α are expressed in HUCB-NSC at all stages of development. During neuronal differentiation of HUCB-NSC by using dBcAMP, 5% oxygen level act synergistically, promoting further differentiation (enhanced MAP2 expression). Application of prolyl hydroxylase inhibitor – DMOG resulted in increased expression of HIF1α but not HIF2α and increased the expression of MAP2 (only in 21% oxygen conditions) referring to variants without DMOG. Sponsored by grant from Polish Ministry of Scientific Research and Higher Education No N N302 597838 and by NSC grant No 2011/01/B/NZ3/05401
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