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1

MiR-378a-5p regulates CAMKK2/AMPK pathway to contribute to cerebral ischemia/reperfusion injury-induced neuronal apoptosis

100%
Zhang Y., Zhang P., Deng C.
Folia Histochemica et Cytobiologica
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2021
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tom 59
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nr 1
2

Fate of glial progenitors is dictated by the local tissue microenvironment

84%
Sypecka J., Sarnowska A.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr 1
The oligodendrocyte progenitors (OPCs) are the abundant population of NG2-positive cells in the young and adult CNS. They are capable of myelinogenesis, but they are also among the first cells to react to CNS injuries. Over the last decade, these glia commited progenitors have been however the subject of intensive research in context of their assumed neural stem cell properties. In our studies we have addressed the question of the impact of the local tissue microenvironment on the OPC commitment and differentiation. Their susceptibility to external stimuli and assumed intrinsic neurogenic potential have been investigated in co-culture models with organotypic slices derived from two distinct CNS regions (hippocampus and spinal cord). The hippocampal slice culture exposed to oxygen glucose deprivation (OGD) was used to evaluate the cell differentiation in microenvironment conditioned by traumatized tissue. The results have shown that the local instructive clues not only trigger the neuronal commitment of oligodendrocyte progenitors, but also govern the oligodendroglial maturation. While the trophic factors secreted by hippocampal slices efficiently promoted neurogenesis, the observed effect was significantly abolished in co-cultures with the OGD-subjected tissue. The less pronounced susceptibility to adopting neuronal phenotype and the considerable slowdown of oligodendroglial differentiation was observed in the co-cultures with the spinal cord slices. Our findings indicate that OPCs actually meet some of the neural stem cell criteria. The obtained results also suggest that the specificity of the instructive clue cocktail might module the fate choice of mobilized endogenous or transplanted cells, which is important while planning neurorepair strategies. Supported by grant 0345/B/P01/2010/38.
3

Leukemia inhibitory factor inhibits the proliferation of primary rat astrocytes induced by oxygen-glucose deprivation

84%
Fan Y.-Y., Zhang J.-M., Wang H., Liu X.-Y., Yang F.-H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr 4
Leukemia inhibitory factor (LIF) is a neuroprotective cytokine that is necessary for the normal development of astrocytes. Oxygen-glucose deprivation (OGD) can induce astrocyte proliferation by increasing hypoxia-inducible factor alpha (HIF- 1a) and vascular endothelial growth factor (VEGF). Here, we studied whether LIF affects the proliferation of cultured primary rat astrocytes under OGD conditions by measuring EdU incorporation into astrocyte DNA and the expression of proliferating cell nuclear antigen (PCNA) mRNA and protein. Our findings show that low concentrations of LIF (5 and 10 ng/mL) significantly decreased EdU incorporation and downregulated the expression of PCNA mRNA and PCNA protein in astrocytes subjected to OGD. A low concentration of LIF (10 ng/mL) clearly inhibited astrocyte proliferation induced by OGD, while a higher concentration (50 ng/mL) had no effect. To investigate the mechanism of this inhibition by LIF (10 ng/ mL), the expression of 3 related genes (LIF receptor, HIF-1a, and VEGF) was assessed using real-time PCR; VEGF protein expression was measured by Western blot. Our results indicate that LIFR mRNA was downregulated in astrocytes subjected to OGD. Interestingly, treatment with LIF further reduced LIFR mRNA expression in these cells. LIF treatment also decreased the expression of HIF-1a mRNA, VEGF mRNA, and VEGF protein induced by OGD. Low concentrations of LIF were observed to inhibit astrocyte proliferation induced by OGD.
4

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.
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