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1

Exploring and manipulating function of microglia in brain pathologies

100%
Kaminska B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Microglia are multifunctional immune cells of the brain executing various functions and rapidly responding to pathological insults. Brain injury, hypoxia, infection or aberrant protein accumulation may lead to chronic infl ammation with a progressive shift in microglia function towards infl ammatory phenotype and accumulation of immune cells. Under pathological conditions, the interplay of extrinsic signals directs microglia towards neuroprotective or detrimental phenotype. Molecular mechanisms of initiation, progression and termination of microglia-initiated infl ammatory responses in the brain, in particular gene networks and signaling pathways are poorly understood. Characterization of the global transcriptome of microglia exposed to infl ammatory or cytoprotective signals and analysis of signalling pathways revealed differences in expression of genes encoding cytokines/ chemokines and transcription regulators. Identifi cation of signalling pathways contributing to discrete microglia phenotypes and discovery of transcription regulators which may serve as “master switches” for induction of an infl ammatory phenotype, will allow to target specifi c functions of microglia. Therapeutic approaches targeting signal transduction in microglia will be discussed. A greater understanding of microglia functions coupled with advances in pharmacology and gene therapy will support development of functionally “engineered” microglia able to convey neuroprotection.
2

Immunohistochemical study of microglia cells during the development of rat brain

100%
Domaradzka-Pytel B., Maciejewska B., Berdel B., Morys J.
Folia Morphologica
|
1998
|
tom 57
|
nr 2
3

Kainic acid induces expression of caveolin-1 in activated microglia in rat brain

84%
Takeuchi S., Matsuda W., Tooyama I., Yasuhara O.
Folia Histochemica et Cytobiologica
|
2013
|
tom 51
|
nr 1
4

Expression of interleukin-16 by tumor-associated macrophages-activated microglia in high-grade astrocytic brain tomors

84%
Liebrich M., Guo L. H., Schluesener H. J., Schwab J. M., Dietz K., Will B. E., Meyermann R.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
tom 55
|
nr 1
5

Ultrastructural evaluation of phagocytic function of perivascular cells and interstitial microglia in the brain of rats surviving one year after cardiac arrest-induced global cerebral ischemia

84%
Walski M., Frontczak-Baniewicz M., Wojewodzka U., Gajkowska B.
Acta Biologica Cracoviensia. Series Zoologia
|
2003
|
tom 45
6

Origin and the functional role of microglia

84%
Wozniak W.
Folia Morphologica
|
1998
|
tom 57
|
nr 4
7

Interrelations between nuclear-factor kappa B activation, glial response and neuronal apoptosis in gerbil hippocampus after ischemia

84%
Domanska-Janik K., Bronisz-Kowalczyk A., Zajac H., Zablocka B.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 1
8
Content available remote

Lipopolysaccharide changes sialylation pattern in the mouse central nervous system

67%
Wielgat P., Holownia A., Braszko J. J.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 5
9

The classification of microglial activation phenotypes on neurodegeneration and regeneration in Alzheimer’s disease brain

67%
Varnum M. M., Ikezu T.
Archivum Immunologiae et Therapiae Experimentalis
|
2012
|
tom 60
|
nr 4
10
Content available remote

Standardized Tribulus terrestris extract protects against rotenone-induced oxidative damage and nigral dopamine neuronal loss in mice

67%
Alzahrani S., Ezzat W., Elshaer R. E., Abd El-Lateef A. S., Mohammad H. M. F., Elkazaz A. Y., Toraih E., Zaitone S. A.
Journal of Physiology and Pharmacology
|
2018
|
tom 69
|
nr 6
11

Phosphatidylserine-containing liposomes: potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E2 after uptake by myeloid derived phagocytes

67%
Wu Z., Nakanishi H.
Archivum Immunologiae et Therapiae Experimentalis
|
2011
|
tom 59
|
nr 3
12

Immunohistochemical analysis of spinal cord components in mouse model of experimental autoimmune encephalomyelitis

67%
Pyka-Fosciak G., Stasiolek M., Litwin J. A.
Folia Histochemica et Cytobiologica
|
2018
|
tom 56
|
nr 3
13
Content available remote

Role of macrophage colony-stimulating factor (M-CSF)-dependent macrophages in gastric ulcer healing in mice

67%
Kawahara Y., Nakase Y., Isomoto Y., Matsuda N., Amagase K., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 4
14

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

67%
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.
15

Synantocytes: the fifth type of glia? In comparison with astrocytes

67%
Krawczyk A., Jaworska-Adamu J.
Folia Histochemica et Cytobiologica
|
2010
|
tom 48
|
nr 2
173-177
16

MHC class II positive microglia and lymhocytic infiltration are present in the substantia nigra and striatum in mouse model of Parkinson's disease

67%
Kurkowska-Jastrzebska I., Wronska A., Kohutnicka M., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 1
17

Brain injury: prolonged induction of transcription factors

51%
Pennypacker K. R., Kassed C. A., Eidizadeh S., O'Callaghan J. P.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 4
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
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