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1

Immunohistochemical study of microglial and astroglial cells during postnatal development of rat striatum

100%
Domaradzka-Pytel B., Ludkiewicz B., Jagalska-Majewska H., Morys J.
Folia Morphologica
|
1999
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tom 58
|
nr 4
The present study investigates the development of microglial and astroglial cells in the postnatal rat striatum, using immunohistochemical methods with panel antibodies that recognize macrophage antigens of unknown function - ED l, complement type 3 receptor- OX-42 (for microglia) and glial fibrillary acidic protein (for astrocytes). On the day of birth, EDl/OX-42- immunoreactive microglial cells present in the striatum represent ameboid microglia. Between PO and P10 we could observe the migration of ameboid microglial cells from neuroepithelial ventricular zone through internal and external capsules into the striatum. During the second postnatal week (PIO, P14) a considerable decline of ameboid EDl-immunoreactive microglial cells and an increase of the number of OX-42 positive ramified cells were observed. At P21 only OX-42 positive ramified cells were observed in the whole striatum. On the day of birth, only a few GFAP positive cells resembling radial glia were observed in the striatium. During the first postnatal week, the number of GFAP-positive cells increased significantly; they showed typical morphology of the astrocytes present in the adult animals. After P22 the final striatal population of astroglia was formed.
2

Paracrine interactions between non-activated N9 microglial cells in co-culture with SN56 cholinergic neuronal cells

86%
Gul-Hinc S., Ronowska A., Bielarczyk H., Szutowicz A.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr 1
Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic exposure to Zn or SNP caused loss of viability (30%), inhibition of pyruvate dehydrogenase (PDH) (40%), isocitrate dehydrogenase (60 and 50%) and aconitase activities as well as decrease of acetyl-CoA levels. These alterations in enzyme activities displayed strong direct correlation with depletion of acetylCoA (r=0.86, P<0.0001) and inverse correlation with cell viability (r=0.87, P<0.0001). Resveratrol, free radical scavenger, increased viability of Zn/SNP treated cholinergic cells but did not overcome suppresive effects of SNP and Zn on enzymes activities. Under same neurotoxic conditions, N9 microglial cells cultured on isoporated inserts and added to neuronal culture dishes, also overcame neurotoxic effect Zn and SNP maintaining control levels of acetyl-CoA, enzymes activites and high cell viability. These data sugest that in some specific, pathologic conditions, non-activated microglia may protect neuronal cholinergic neurons against neurotoxic insults by paracrine-like mechanism by protecting their energy metabolism. On the other hand resveratrol neuroprotection may depend on entirely different yet undefined mechanism. Supported by GUMed MN-15, MNiSW NN401029937, IP2010035370, GUMed ST-57 projects.
3

Microglial expression of peptidylarginine deiminase 2 in the prenatal rat brain

72%
Asaga H., Ishigami A.
Cellular and Molecular Biology Letters
|
2007
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tom 12
|
nr 4
536-544
Peptidylarginine deiminases (PADs) are Ca2t+-dependant post-translational modification enzymes that catalyze the citrullination of protein arginyl residues. PAD type 2 (PAD2) is thought to be involved in some processes of neurodegeneration and myelination in the central nervous system. In this study, we found PAD2-positive cells in rat cerebra in 19-to 21-day old embryos, i.e. at a developmental stage well before myelination begins. Most of the cells were microglial marker-positive cells found mainly in the prospective medulla, and others were microglial marker-negative cells found mainly in the prospective dentate gyrus of the hippocampus. The former seemed to be in an activated state as judged by morphological criteria. The specificity of the enzyme activity, immunoblotting and reverse transcriptase-polymerase chain reaction analyses revealed that these cells expressed PAD2 and not PAD1, PAD3 or PAD4. Our data is indicative of microglial expression of PAD2 in the prenatal developing cerebrum.
4

Origin and the functional role of microglia

72%
Wozniak W.
Folia Morphologica
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1998
|
tom 57
|
nr 4
5

Mechanisms of immune regulation in Alzheimer's disease: a viewpoint

72%
Marx F., Blasko I., Grubeck-Loebenstein B.
Archivum Immunologiae et Therapiae Experimentalis
|
1999
|
tom 47
|
nr 4
6

Microglial and astroglial cells in the rat paraclaustral reservoir during postnatal development: an immunohistochemical study

72%
Ludkiewicz B., Domaradzka-Pytel B., Morys J.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 1
7

The role of microglia cells activation in the effects of opioids

58%
Popiolek-Barczyk K., Rojewska E., Zychowska M., Makuch V., Przewlocka B., Mika J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Development of neuropathic pain is accompanied by many changes in immune and glial cells. These changes correspond to activation of immune and glial cells that have been shown to influence the opioid effectiveness and can be modulated by minocycline (a potent inhibitor of microglial activation). In earlier study we have demonstrated that function of opioidergic neurons may be modulated by the immune system. These changes have been shown to be responsible for the efficacy of opioids. The aim of our study was to examine the effect of the minocycline-triggered inhibition of microglia activation on the injury-induced changes and the efficacy of mu and delta opioid receptor ligands in a rat model of neuropathic pain (chronic constriction injury to the sciatic nerve). In cell culture studies, we examined the influence of opioids (morphine, DAMGO, DPDPE, deltorphin II) on activated primary cultured rat microglia by using MTT and/or NO assays. All experiments were performed according to the IASP recommendations and were approved by a local Bioethics Committee. On the spinal cord level the injury to the sciatic nerve induced an up-regulation of IL-1beta, IL-6 expression, CX3CR1 and C1q (marker of microglia, macrophage and leukocyte activation). Chronic administration of minocycline not only diminished neuropathic pain-related behavior and C1q-positive cell activation, but also attenuate the changes in proinflammatory factors like IL1beta, IL-6 and CX3CR1 in the spinal cord and DRG. In in vivo experiments, the analgesic effects of mu-opioid (morphine and DAMGO), but not delta-opioid (DPDPE, deltorphin II) receptor ligands were lower in the rats under neuropathic pain. Moreover, the analgesic effects of morphine and DAMGO, but not DPDPE and deltorphin II were significantly potentiated by minocycline chronic administration. Our in vitro findings that non-stimulated microglia cells respond differently to opioids in comparisons with stimulated cells as measured by MTT and/or NO assays, corresponded well with the results of in vivo studies. Our study underlined that inhibition of microglial activation could differently influence analgesic effects of mu- but not delta-opioid ligands in injury-induced pathologies, which may influence the effect of various opioid drugs used in chronic pain therapy.
8

Expression of the transcription factor regulatory factor X1 in the mouse brain

58%
Feng C., Li J., Zuo Z.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 2
9

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

58%
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.
10
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The role of oligodendrocytes in chronic pain: cellular and molecular mechanisms

58%
Malta I., Moraes T., Rodrigues G., Franco P., Galdino G.
Journal of Physiology and Pharmacology
|
2019
|
tom 70
|
nr 5
11

Cathepsin E (EC 3.4.23.34) — a review

51%
Chlabicz M., Gacko M., Worowska A., Lapinski R.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 4
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