Migration of enhanced green fluorescent protein expressing bone marrow-derived microglia/macrophage into the mouse brain following permanent focal ischemia

Tanaka, Ryota; Komine-Kobayashi, Miki; Mochizuki, Hideki; Yamada, Masanori; Furuya, Tsuyoshi; Migita, Makoto; Shimada, Takashi; Mizuno, Yoshikuni; Urabe, Takao

doi:10.1016/s0306-4522(02)00954-5

Cited by 217 publications

(172 citation statements)

References 48 publications

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“…In the normal brain, IBA-1 is highly expressed in resident microglial cells, but is never expressed in neurons and astrocytes [22]. After ischemia, IBA-1 is also expressed in activated resident microglial cells and infiltrating hematogenous macrophages [23,24]. …”

Section: Discussionmentioning

confidence: 99%

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

et al. 2010

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Background Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia. Results Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals. Conclusion These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.

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Section: Discussionmentioning

confidence: 99%

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

et al. 2010

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“…To continue the exploration of the uses of exogenous microglia, we are currently isolating microglia from bone marrow (Ono et al, 1999;Tanaka et al, 2003). In the future, the administration of microglia might be a potential tool for cell or gene therapy in the treatment of brain disease.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Imai

Suzuki

Oda

et al. 2006

J Cereb Blood Flow Metab

189

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Exogenous microglia pass through the blood-brain barrier and migrate to ischemic hippocampal lesions when injected into the circulation. We investigated the effect of exogenous microglia on ischemic CA1 pyramidal neurons. Microglia were isolated from neonatal mixed brain cultures, labeled with the fluorescent dye PKH26, and injected into the subclavian artery of Mongolian gerbils subjected to ischemia reperfusion neuronal injury. PKH26-labeled microglia migrated to the ischemic hippocampal lesion, resulting in increased numbers of surviving neurons compared with control animals, even when injected 24 h after ischemia. Interferon-c stimulation of isolated microglia enhanced the neuroprotective effect. Administration of exogenous microglia resulted in normal performance in a passive avoidance-learning task. Additionally, administration of exogenous microglia increased the expression of brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor in the ischemic hippocampus, and thus might have induced neurotrophin-dependent protective activity in damaged neurons. Peripherally injected microglia exhibited a specific affinity for ischemic brain lesions, and protected against ischemic neuronal injury in vivo. It is possible that administration of exogenous microglia can be developed as a potential candidate therapy for central nervous system repair after transitory global ischemia.

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“…Several lines of evidence suggest that tissue injury enhances the recruitment of haematopoietic stem cells, mescenchymal stem cells, or their progeny towards a non-haematopoietic fate [11,14,15,16]. This might be because migration of bone marrow stem cells throughout the body essentially act as a back-up system to augment each organ's intrinsic regenerative capacity.…”

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confidence: 99%

“…To elucidate the potential of bone marrow-derived cells for use as beta-cell replacement therapy, we established chimeric mice with the bone marrow of transgenic mice constitutively expressing enhanced green fluorescent protein (EGFP) [16,21,22,23]. As we showed previously, the bone marrow of these chimeric mice is almost completely reconstituted with EGFP-positive cells 5 weeks after transplantation [22].…”

mentioning

confidence: 99%

Little evidence of transdifferentiation of bone marrow-derived cells into pancreatic beta cells

et al. 2003

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Migration of enhanced green fluorescent protein expressing bone marrow-derived microglia/macrophage into the mouse brain following permanent focal ischemia

Cited by 217 publications

References 48 publications

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

Neuroprotective Effect of Exogenous Microglia in Global Brain Ischemia

Little evidence of transdifferentiation of bone marrow-derived cells into pancreatic beta cells

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