Microtubule-associated protein 2 as a sensitive marker for cerebral ischemic damage—Immunohistochemical investigation of dendritic damage

Kitagawa, Kazuo; Matsumoto, Masayasu; Niinobe, Michio; Mikoshiba, Katsuhiko; Hata, Ryuji; Ueda, Hirokazu; Handa, N.; Fukunaga, Ryuzo; Isaka, Yoshinari; Kimura, Kazufumi; Kamada, Takenobu

doi:10.1016/0306-4522(89)90383-7

Cited by 299 publications

(116 citation statements)

References 18 publications

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“…With these conventional methods, morphological evidence of neuronal death does not become apparent until 1 to 2 hours after the onset of cerebral ischemia. However, early ischemic lesions can now be detected by applying immunohistochemical methods, and a reduction in microtubule-associated protein 2 (MAP2) immunoreactivity has been found to be an early, sensitive marker of ischemic neuronal damage [6]. In our study, by using this method, we showed that the lateral vestibular nucleus (LVe) and the ventral part of the spinal trigeminal nucleus (vSp5) were particularly vulnerable to ischemia.…”

Section: Discussionmentioning

confidence: 77%

“…Therefore, ischemia-induced loss of immunoreaction for MAP2 is considered to be a reliable marker of neurons that are already undergoing irreversible processes in cell death [20]. However, Kitagawa et al showed that loss of MAP2 immunostaining preceded the development of overt neuronal loss in a gerbil model of transient forebrain ischemia [6]. Our results are also consistent with this notion that MAP2 immunostaining can be used as an indicator of still viable neurons that will undergo irreversible injury only at a later time point.…”

Section: Discussionmentioning

confidence: 99%

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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: 77%

Section: Discussionmentioning

confidence: 99%

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

et al. 2010

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“…6F). Loss of MAP2 has been considered as an early marker for neuronal damage following cerebral ischemia (25), spinal cord injury (26), and traumatic brain injury (27); therefore, potential toxicities of FUS G156E and FUS P525L to neurons would be reflected by reduced intensity of MAP2 immunostaining in primary neurons. In addition, primary neurons expressing HA-FUS G156E and HA-FUS P525L often exhibited abnormal cell shapes (e.g.…”

Section: Purification and Aggregation Of Gst-fus-his Proteins A Ementioning

confidence: 99%

Intranuclear Aggregation of Mutant FUS/TLS as a Molecular Pathomechanism of Amyotrophic Lateral Sclerosis

Nomura

Watanabe

Kaneko

et al. 2014

Journal of Biological Chemistry

122

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Background: Abnormal accumulation of mutant FUS/TLS is a pathological change in patients with amyotrophic lateral sclerosis (ALS). Results: A pathogenic mutation, G156E, increases propensities of FUS/TLS for aggregation in vitro and in vivo. Conclusion: Intranuclear aggregation of mutant FUS/TLS is a molecular pathomechanism of ALS. Significance: A loss of functional TLS/FUS in the nucleus will lead to neurodegeneration.

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“…T 2-weighted MRI reflects the increased water content in the edematous tissue which consist of damaged neurons and glial cells, while MAr2 immunostaining has been used for the early detection of ischemic neuronal damage (9). Therefore, it is thought that MRI reflects the decline and viability of both neurons and glias while MAr2-staining reflects those of only neurons.…”

Section: Resultsmentioning

confidence: 99%

Effects of Neopterin on Focal Cerebral Ischemia In Rats

et al. 1996

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SummaryWe examined the effects of neopterin on focal cerebral ischemia induced by transient (2 h) occlusion of the middle cerebral artery (MCA) in rats.Neopterin was administered 10 min before reperfusion (3 mg/kg i.p). The ischemic damage was evaluated one week after the MCA occlusion by magnetic resonance imaging (MRI) and by the immunohistochemical reaction for microtubule-associated protein 2 (MAP2). The ischemic lesion detected by MRI was significantly smaller in the neopterin-treated group than in the non-treated group (n=4 in each group, p<0.05). However, the ischemic neuronal damage determined by MAP2 in the neopterintreated group was not significantly different from that in the non-treated group. Since MRI is thought to reflect the distribution of not only neurons but also glial cells, these results may indicate the effects of neopterin on the glial reaction in focal cerebral ischemia.

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Microtubule-associated protein 2 as a sensitive marker for cerebral ischemic damage—Immunohistochemical investigation of dendritic damage

Cited by 299 publications

References 18 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

Intranuclear Aggregation of Mutant FUS/TLS as a Molecular Pathomechanism of Amyotrophic Lateral Sclerosis

Effects of Neopterin on Focal Cerebral Ischemia In Rats

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