CNS neuroscience & therapeutics · 2011
Deficiency of NG2+ cells contributes to the susceptibility of stroke-prone spontaneously hypertensive rats.
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Wang Pei, Tian Wei-Wei, Song Jie, Guan Yun-Feng, Miao Chao-Yu
Аннотация
AIMS: The purpose of this study is to investigate whether the NG2(+) cells, a class of oligodendrocyte progenitor cells, is involved in the pathophysiology of stroke in stroke-prone spontaneously hypertensive rat (SHR-SP).
METHODS: SHR-SP, SHR, Wistar-Kyoto rats (WKY), and C57BJ/6 mice were used. Immunohistochemistry was conducted to evaluate the number of NG2(+) cells in frozen brain sections. Demyelination was evaluated by Sudan black staining and serum level of myelin basic protein. Middle cerebral artery occlusion (MCAO) was performed to prepare experimental stroke model.
RESULTS: The number of NG2(+) cells was significantly decreased in infarct core and increased in penumbra in WKY rats after MCAO. In brain sections of 6-month-old SHR-SP, the number of NG2(+) cells was significantly (P < 0.01) less than that in age-matched SHR and WKY rats. However, this phenomenon was not observed in 3-month-old rats. Demyelination was found in 6-month-old SHR-SP but not in 3-month-old SHR-SP. Pharmacological treatment of cuprizone in mice induced demyelination and enlargement of cerebral infarction after MCAO.
CONCLUSION: The decline of NG2(+) cells may cause demyelination and contribute to the susceptibility of SHR-SP to ischemic brain injury.
METHODS: SHR-SP, SHR, Wistar-Kyoto rats (WKY), and C57BJ/6 mice were used. Immunohistochemistry was conducted to evaluate the number of NG2(+) cells in frozen brain sections. Demyelination was evaluated by Sudan black staining and serum level of myelin basic protein. Middle cerebral artery occlusion (MCAO) was performed to prepare experimental stroke model.
RESULTS: The number of NG2(+) cells was significantly decreased in infarct core and increased in penumbra in WKY rats after MCAO. In brain sections of 6-month-old SHR-SP, the number of NG2(+) cells was significantly (P < 0.01) less than that in age-matched SHR and WKY rats. However, this phenomenon was not observed in 3-month-old rats. Demyelination was found in 6-month-old SHR-SP but not in 3-month-old SHR-SP. Pharmacological treatment of cuprizone in mice induced demyelination and enlargement of cerebral infarction after MCAO.
CONCLUSION: The decline of NG2(+) cells may cause demyelination and contribute to the susceptibility of SHR-SP to ischemic brain injury.