Cytoplasmic translocation of Olig2 in adult glial progenitors marks the generation of reactive astrocytes following autoimmune inflammation

Cassiani-Ingoni, Riccardo; Coksaygan, Turhan; Han, Xue; Reichert-Scrivner, Susan; Wiendl, Heinz; Rao, Mahendra S.; Magnus, Tim

doi:10.1016/j.expneurol.2006.04.030

Cited by 64 publications

(70 citation statements)

References 62 publications

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“…In the neocortex, Olig2-positive cells increase and display Olig2 transcriptional upregulation after acute stab lesion, middle cerebral artery occlusion and upon chronic amyloid plaque deposition [12] . Similar findings are reported after traumatic injuries, demyelination or immune-mediated injury in the striatum, brain stem and spinal cord [27][28][29] . Thus, Olig2 induction is a pan-lesion phenomenon that occurs throughout the CNS.…”

Section: Olig2 Induction Is a Pan-lesion Phenomenonsupporting

confidence: 76%

Fate Determinant Expression in the Lesioned Brain: Olig2 Induction and Its Implications for Neuronal Repair

Buffo

2007

Neurodegener Dis

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Although stem cells persist in restricted regions of the adult mammalian central nervous system (CNS), replacement of neurons does not take place in most regions in intact conditions or after injury. In the last years, proliferative multipotent cells have been isolated from the parenchyma of many CNS regions considered constitutively nonneurogenic, suggesting that the nonneurogenic CNS parenchyma is endowed with a latent neurogenic potential that might be exploited for neuronal replacement. However, neurogenic fate determinants acting during development and in the germinative zones are not expressed in the intact brain and after lesion, thus arguing against the presence of neurogenic competence in parenchymal precursors. Conversely, the basic helix-loop-helix transcription factor Olig2 is widely expressed in subsets of glia cells and progenitors, and it is strongly induced at different sites by both acute and chronic injury, albeit with different mechanisms. Antagonizing Olig2 function in cells proliferating after an acute lesion leads to the upregulation of the neurogenic determinant Pax6 and results in a significant number of newly generated immature neurons. Therefore, Olig2 acts as a repressor of neurogenesis in cells reacting to brain injury. Finding the proper way to fully derepress the neurogenic determinants in these cells, together with providing favorable environmental signals, may represent an effective approach towards evoking neuronal repair from parenchymal precursors.

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Section: Olig2 Induction Is a Pan-lesion Phenomenonsupporting

confidence: 76%

Fate Determinant Expression in the Lesioned Brain: Olig2 Induction and Its Implications for Neuronal Repair

Buffo

2007

Neurodegener Dis

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“…In the adult brain, the translocation of Olig2 into the cytoplasm is found in the process of astroglial activation during brain injury and inflammation (Cassiani-Ingoni et al, 2006;Magnus et al, 2007). All these suggest that the downregulated Olig2 expression and its translocation into cytoplasma are associated with the maturation and activation of astrocytes.…”

Section: Effects Of Hyperforin On Development Of Oligodendrocytesmentioning

confidence: 91%

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Wang

Zhang

et al. 2011

Journal of Neurochemistry

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Major depressive disorder is a common severe psychiatric disorder with unknown etiology. Recent studies show that the loss and malfunction of oligodendrocytes are closely related to the neuropathological changes in depression, which can be reversed by antidepressant treatment. St. John's wort is an effective and safe herbal treatment for depression in several clinical trials. However, the underlying mechanism of its therapeutic effects is unclear. In this study, we evaluated the effects of hyperforin, a iii ACKNOWLEDGEMENTS

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“…We also observed cells being not microglial cells (eGFP-negative cells) that are immunoreactive for MHC class II antibody. It is important to note that MHC class II complex can also be expressed by other cell types in the CNS, as, for example, by NG2 1 progenitor cells (Cassiani-Ingoni et al, 2006). Mac-2 immunostaining suggest that microglial cells accumulated in the area of the LMC at E13.5 and E14.5 are in an activated state, which might be related to particular developmental processes, such as DCD.…”

Section: Activation States Of Microglial Cells In the Developing Embrmentioning

confidence: 99%

Pattern of invasion of the embryonic mouse spinal cord by microglial cells at the time of the onset of functional neuronal networks

Rigato

Buckinx

Le-Corronc

et al. 2011

Glia

131

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Microglial cells invade the central nervous system during embryonic development, but their developmental functional roles in vivo remain largely unknown. Accordingly, their invasion pattern during early embryonic development is still poorly understood. To address this issue, we analyzed the initial developmental pattern of microglial cell invasion in the spinal cord of CX3CR1-eGFP mouse embryos using immunohistochemistry. Microglial cells began to invade the mouse embryonic spinal cord at a developmental period corresponding to the onset of spontaneous electrical activity and of synaptogenesis. Microglial cells reached the spinal cord through the peripheral vasculature and began to invade the parenchyma at 11.5 days of embryonic age (E11.5). Remarkably, at E12.5, activated microglial cells aggregated in the dorsolateral region close to terminals of dying dorsal root ganglia neurons. At E13.5, microglial cells in the ventral marginal zone interacted with radial glial cells, whereas ramified microglial cells within the parenchyma interacted with growing capillaries. At this age, activated microglial cells (Mac-2 staining) also accumulated within the lateral motor columns at the onset of the developmental cell death of motoneurons. This cell aggregation was still observed at E14.5, but microglial cells no longer expressed Mac-2. At E15.5, microglial cells were randomly distributed within the parenchyma. Our results provide the essential basis for further studies on the role of microglial cells in the early development of spinal cord neuronal networks in vivo.

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Cytoplasmic translocation of Olig2 in adult glial progenitors marks the generation of reactive astrocytes following autoimmune inflammation

Cited by 64 publications

References 62 publications

Fate Determinant Expression in the Lesioned Brain: Olig2 Induction and Its Implications for Neuronal Repair

Fate Determinant Expression in the Lesioned Brain: Olig2 Induction and Its Implications for Neuronal Repair

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Pattern of invasion of the embryonic mouse spinal cord by microglial cells at the time of the onset of functional neuronal networks

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