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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cell type-specific activation of p38 MAPK in the brain regions of hypoxic preconditioned mice.
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Cell type-specific activation of p38 MAPK in the brain regions of hypoxic preconditioned mice.

机译：低氧预适应小鼠脑区域中p38 MAPK的细胞类型特异性激活。

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Activation of p38 mitogen-activated protein kinase (p38 MAPK) has been implicated as a mechanism of ischemia/hypoxia-induced cerebral injury. The current study was designed to explore the involvement of p38 MAPK in the development of cerebral hypoxic preconditioning (HPC) by observing the changes in dual phosphorylation (p-p38 MAPK) at threonine180 and tyrosine182 sites, protein expression, and cellular distribution of p-p38 MAPK in the brain of HPC mice. We found that the p-p38 MAPK levels, not protein expression, increased significantly (p<0.05) in the regions of frontal cortex, hippocampus, and hypothalamus of mice in response to repetitive hypoxic exposure (H1-H6, n=6 for each group) when compared to values of the control normoxic group (H0, n=6) using Western blot analysis. Similar results were also confirmed by an immunostaining study of the p-p38 MAPK location in the frontal cortex, hippocampus, and hypothalamus of mice from HPC groups. To further define the cell type of p-p38 MAPK positive cells, we used a double-labeled immunofluorescent staining method to co-localize p-p38 MAPK with neurofilaments heavy chain (NF-H, neuron-specific marker), S100 (astrocyte-specific marker), and CD11b (microglia-specific maker), respectively. We found that the increased p-p38 MAPK occurred in microglia of cortex and hippocampus, as well as in neurons of hypothalamus of HPC mice. These results suggest that the cell type-specific activation of p38 MAPK in the specific brain regions might contribute to the development of cerebral HPC mechanism in mice.
机译：p38丝裂原活化蛋白激酶（p38 MAPK）的激活已被认为是缺血/缺氧引起的脑损伤的机制。本研究旨在通过观察苏氨酸180和酪氨酸182位点的双重磷酸化（p-p38 MAPK）的变化，蛋白表达和p-38细胞分布来探索p38 MAPK在脑缺氧预处理（HPC）发育中的参与。 HPC小鼠大脑中的p38 MAPK。我们发现p-p38 MAPK水平而非蛋白表达在小鼠的额叶皮层，海马和下丘脑区域显着增加（p <0.05），以应对反复的低氧暴露（H1-H6，每组n = 6）使用Western blot分析与正常氧正常对照组（H0，n = 6）的值进行比较。对HPC组小鼠的额叶皮层，海马和下丘脑中p-p38 MAPK位置的免疫染色研究也证实了类似的结果。为了进一步定义p-p38 MAPK阳性细胞的细胞类型，我们使用了双重标记的免疫荧光染色方法将p-p38 MAPK与神经丝重链（NF-H，神经元特异性标记），S100（星形胶质细胞特异性标记）和CD11b（小胶质细胞特异性标记）。我们发现增加的p-p38 MAPK发生在皮质和海马小胶质细胞以及HPC小鼠下丘脑神经元中。这些结果表明，特定脑区域中p38 MAPK的细胞类型特异性激活可能有助于小鼠脑HPC机制的发展。

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