Responses of microglia and neural progenitors to mechanical brain injury

Tzeng, Shun-Fen; Wu, Jen Pey

doi:10.1097/00001756-199908020-00012

Cited by 54 publications

(31 citation statements)

References 11 publications

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“…Previous studies have shown that there is an increased proliferation of precursor cells in this zone after injury (Weinstein et al, 1996;Tseng and Wu, 1999;Jin et al, 2001). Interestingly, we found MIB5-IR cells in close apposition to Mts1-positive astrocytes with low levels of GFAP, as well as to intensely GFAPlabeled cells, which did not express Mts1.…”

Section: Discussionmentioning

confidence: 94%

Mts1 protein expression in the central nervous system after injury

Kozlova

Lukanidin

2002

Glia

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We recently showed that Mts1 is expressed in white matter astrocytes in the rat brain and spinal cord from the first postnatal day. Its expression level declined in the adult CNS, but its topographical localization was maintained. Only white matter astrocytes in the cerebellum did not express Mts1. After dorsal root or sciatic nerve injury, we observed a marked upregulation of Mts1 in the area of the dorsal funiculus undergoing Wallerian degeneration. Here we show that upregulation of Mts1 is a consistent feature of astrocytes in white matter undergoing Wallerian degeneration. In addition, Mts1 is upregulated in astrocytes outlining the lesion site of a penetrating injury to the forebrain, or cerebellum. Gray matter astrocytes did not express Mts1, even after direct injury. In injured brain, we consistently noted a close relationship between Mts1-expressing astrocytes and ED1-positive microglia/macrophages, which are known to be highly motile cells. Mts1 was expressed in the periventricular area and the rostral migratory stream, i.e., sites of ongoing neuroplasticity in adulthood, and was upregulated in these areas after injury. These data suggest that Mts1-expressing astrocytes play a significant role in degenerative events in the mature white matter, interact with phagocytic microglia/macrophages and regulate cell migration and differentiation in areas of the adult brain with a high degree of plasticity.

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Section: Discussionmentioning

confidence: 94%

Mts1 protein expression in the central nervous system after injury

Kozlova

Lukanidin

2002

Glia

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“…Stroke elicits a robust response in the SVZ (Arvidsson et al, 2002) and it is not clear if a similar response is seen after stab wound injury (Synowitz et al, 2006;Tzeng and Wu, 1999). As such, the different cellular responses observed in response to injury may underlie the differences reported.…”

Section: Discussionmentioning

confidence: 99%

Adult Neural Stem Cells from the Subventricular Zone Give Rise to Reactive Astrocytes in the Cortex after Stroke

et al. 2015

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Reactive astrocytes (RAs) have been reported to convert to multipotent neural stem cells (NSCs) capable of neurosphere (NS) formation and multilineage differentiation in vitro. Using genetic tagging, we determined that subventricular zone (SVZ) NSCs give rise to NSs derived from the stroke-injured cortex. We demonstrate that these cells can be isolated from the cortex in two different models of stroke and from different stroke-lesioned cortical regions. Interestingly, SVZ NSCs give rise to a subpopulation of RAs in the cortex that contribute to astrogliosis and scar formation. Last, we show that these SVZ derived RAs can be converted to neurons in vivo by forced expression of Ascl1. Identifying the contribution of cells originating from the SVZ to injury repair has implications for neural regeneration strategies.

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“…In the absence of a known mechanism for ischemia-induced neurogenesis and because possible mechanisms include trans-synaptic and diffusible chemical effects, it is unclear if either finding should be surprising. Contralateral electrical, chemical, and vascular effects of hemispheric ischemia are well described, and bilateral induction of neurogenesis by a unilateral stimulus has been reported (22,43). Unilateral stimulation of the perforant path, leading to focal seizure discharges without neuronal injury, increases neurogenesis in the SGZ both ipsilateral and contralateral to the stimulated side (22), and traumatic injury to the cerebral cortex increases BrdUrd labeling in the SVZ bilaterally (43).…”

Section: Discussionmentioning

confidence: 99%

“…Contralateral electrical, chemical, and vascular effects of hemispheric ischemia are well described, and bilateral induction of neurogenesis by a unilateral stimulus has been reported (22,43). Unilateral stimulation of the perforant path, leading to focal seizure discharges without neuronal injury, increases neurogenesis in the SGZ both ipsilateral and contralateral to the stimulated side (22), and traumatic injury to the cerebral cortex increases BrdUrd labeling in the SVZ bilaterally (43). Because transplanted neural stem cells can migrate into tumors from the contralateral hemisphere (44), endogenous neuronal precursors might be expected to proliferate in response to contralateral ischemia as well.…”

Section: Discussionmentioning

confidence: 99%

Neurogenesis in dentate subgranular zone and rostral subventricular zone after focal cerebral ischemia in the rat

Jin

Minami

Lan

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

972

678

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Because neurogenesis persists in the adult mammalian brain and can be regulated by physiological and pathological events, we investigated its possible involvement in the brain's response to focal cerebral ischemia. Ischemia was induced by occlusion of the middle cerebral artery in the rat for 90 min, and proliferating cells were labeled with 5-bromo-2 -deoxyuridine-5 -monophosphate (BrdUrd) over 2-day periods before sacrificing animals 1, 2 or 3 weeks after ischemia. Ischemia increased the incorporation of BrdUrd into cells in two neuroproliferative regions-the subgranular zone of the dentate gyrus and the rostral subventricular zone. Both effects were bilateral, but that in the subgranular zone was more prominent on the ischemic side. Cells labeled with BrdUrd coexpressed the immature neuronal markers doublecortin and proliferating cell nuclear antigen but did not express the more mature cell markers NeuN and Hu, suggesting that they were nascent neurons. These results support a role for ischemia-induced neurogenesis in what may be adaptive processes that contribute to recovery after stroke. D iseases of the brain have singularly adverse effects on the quality and duration of life. Unlike many other tissues, the mature brain has limited regenerative capacity, and its unusual degree of cellular specialization restricts the extent to which residual healthy tissue can assume the function of damaged brain. However, cerebral neurons are derived from precursor cells that persist in the adult brain (1-5), so stimulation of endogenous neural precursors in the adult brain could have therapeutic potential (6).Neurogenesis occurs in discrete regions of the adult brain, including the rostral subventricular zone (SVZ) of the lateral ventricles (7) and the subgranular zone (SGZ) of the dentate gyrus (DG) (8). Neurons that arise in the SVZ travel via the rostral migratory stream to the olfactory bulb (9) and also enter association neocortex (10), and new neurons leaving the SGZ migrate into the adjacent DG granule cell layer. Neurogenesis in these regions is subject to physiological regulation by glucocorticoids (11), sex hormones (12), growth factors (13-16), excitatory neurotransmission (17), learning (18), and stress (19) and can be modified pharmacologically (20).Pathological events can also stimulate neurogenesis in the adult brain. Mechanical injury to the DG granule cell layer in the rat increases proliferation of granule neuron precursors in the adjacent SGZ, as shown by enhanced incorporation of [ 3 H]thymidine and 5-bromo-2Ј-deoxyuridine-5Ј-monophosphate (BrdUrd), induction of proliferating cell nuclear antigen (PCNA), and coexpression of mature neuronal markers in [ 3 H]thymidinelabeled cells (21). Seizures also trigger neurogenesis in the SGZ, with BrdUrd-labeled cells expressing the neuronal markers TOAD-64, class III␤-tubulin, and microtubule-associated protein 2 (MAP-2) (22). Finally, apoptosis induced by oxidative stress in mouse corticothalamic neurons increases BrdUrd labeling in cells that go on to express ...

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Responses of microglia and neural progenitors to mechanical brain injury

Cited by 54 publications

References 11 publications

Mts1 protein expression in the central nervous system after injury

Mts1 protein expression in the central nervous system after injury

Adult Neural Stem Cells from the Subventricular Zone Give Rise to Reactive Astrocytes in the Cortex after Stroke

Neurogenesis in dentate subgranular zone and rostral subventricular zone after focal cerebral ischemia in the rat

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