High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.
High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.
复制标题
高糖上调肌球蛋白轻链激酶诱导海马神经元微丝细胞骨架重排
DOI：
10.3892/mmr.2018.8960
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发表时间：
2018-07
影响因子：
3.4
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Zhu L;Li C;Du G;Pan M;Liu G;Pan W;Li X
慢性高血糖导致肌球蛋白轻链激酶（MLCK）上调并诱导神经元损伤。然而，高血糖症神经元损伤的分子机制尚未完全阐明。在本研究中，海马神经元细胞培养和处理与高浓度的葡萄糖（45 mmol/l）。结果表明，高糖可引起突触萎缩，核形态不规则，微丝损伤。细胞凋亡率增加，MLCK和磷酸化（p）-MLC蛋白表达上调。MLCK抑制剂ML-7在很大程度上逆转了微丝细胞骨架的改变，抑制了F-actin解聚，减少了细胞凋亡，下调了MLCK和p-MLC蛋白的表达。总之，这些结果表明，高糖上调MLCK，促进F-actin解聚，诱导海马神经元细胞微丝骨架重排。
Chronic hyperglycemia leads to myosin light chain kinase (MLCK) upregulation and induces neuronal damage. However, the underlying molecular mechanism of neuronal damage in hyperglycemia has not yet been fully elucidated. In the present study, hippocampal neuronal cells were cultured and treated with a high glucose concentration (45 mmol/l). The results demonstrated that high glucose induced shrinking of the synapses, nuclear shape irregularity and microfilament damage. Filamentous actin (F-actin) filaments were rearranged, cell apoptosis rate was increased and the protein expression of MLCK and phosphorylated (p)-MLC was upregulated. The MLCK inhibitor ML-7 largely reversed the alterations in the microfilament cytoskeleton, inhibited F-actin depolymerization, reduced apoptosis and downregulated MLCK and p-MLC protein expression. Overall, these results indicated that high glucose upregulated MLCK to promote F-actin depolymerization, which induced microfilament cytoskeleton rearrangement in hippocampal neuronal cells.
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