کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6262315 1292351 2016 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research reportRegulation and role of ERK phosphorylation in glial cells following a nigrostriatal pathway injury
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Research reportRegulation and role of ERK phosphorylation in glial cells following a nigrostriatal pathway injury
چکیده انگلیسی


- The nigrostriatal pathway injury affects the proliferation and activation of glial cells.
- P-ERK was located in glial cells at different time points after brain injury.
- U0126 attenuates p-ERK expression and proliferation and activation of glial cells after injury.
- U0126 improved long-term neurobehavioral function after brain injury.

This study was undertaken to examine the function of extracellular signal-regulated kinase (ERK) signaling pathway on the proliferation and activation of microglia/macrophage and astrocytes after brain injury in mice. The result of Western blot showed that p-ERK was immediately activated after injury (<4 h), but the duration was short (<4 days). According to immunofluorescence double staining, it was found that at 4 and 8 h after injury, p-ERK was expressed in microglia/macrophages, and that more cells were co-expressed by p-ERK and IBA-1 (microglia/macrophage marker) at 8 h; at days 1 and 4, p-ERK was expressed in astrocytes, and more cells were co-expressed by p-ERK and GFAP (astrocyte marker) at day 4. After injury, the mice were injected with U0126 (MAPK/ERK signaling pathway inhibitor) via the femoral vein. Compared with those injected with DMSO, the cell number co-expressed by p-ERK and IBA-1 or GFAP significantly decreased (P<0.05). The increase of microglia/macrophage and astrocyte caused by injury was remitted, and the positive cell number significantly decreased (P<0.05). Western blot showed that the expression quantity of IBA-1 and GFAP significantly decreased (P<0.05). Furthermore, the ERK signaling pathway was involved in the proliferation and activation of the two glial cells types and improved long-term neurobehavioral function after brain injury. Therefore, the exploration of the formation mechanism of glial scar after injury and further research on the therapeutic method of neural regeneration are essential.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1648, Part A, 1 October 2016, Pages 90-100
نویسندگان
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