Oligodendrocyte degeneration and recovery after focal cerebral ischemia.
Oligodendrocyte degeneration and recovery after focal cerebral ischemia.
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DOI:
10.1016/j.neuroscience.2010.04.070
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发表时间:
2010-09-01
期刊:
影响因子:
3.3
通讯作者:
Goldberg, M. P.
中科院分区:
文献类型:
--
作者:
McIver, S. R.;Muccigrosso, M.;Gonzales, E. R.;Lee, J. M.;Roberts, M. S.;Sands, M. S.;Goldberg, M. P.
The vulnerability of oligodendrocytes to ischemic injury may contribute to functional loss in diseases of central white matter. Immunocytochemical methods to identify oligodendrocyte injury in experimental models rely on epitope availability, and fail to discriminate structural changes in oligodendrocyte morphology. We previously described the use of a lentiviral vector (LV) carrying eGFP under the myelin basic protein (MBP) promoter for selective visualization of oligodendrocyte cell bodies and processes. In this study, we used LV-MBP-eGFP to label oligodendrocytes in rat cerebral white matter prior to transient focal cerebral ischemia, and examined oligodendrocyte injury 24 hours, 48 hours and one week post-reperfusion by quantifying cell survival and assaying the integrity of myelin processes. There was progressive loss of GFP+ oligodendrocytes in ischemic white matter at 24 and 48 hrs. Surviving GFP+ cells had non-pyknotic nuclear morphology and were TUNEL-negative, but there was marked fragmentation of myelin processes as early as 24 hours after stroke. One week after stroke, we observed a restoration of GFP+ oligodendrocytes in ischemic white matter, reflected both by cell counts and by structural integrity of myelin processes. Proliferating cells were not the main source of GFP+ oligodendrocytes, as revealed by BrdU incorporation. These observations identify novel transient structural changes in oligodendrocyte cell bodies and myelinating processes, which may have consequences for white matter function after stroke.
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