ArticleMolecular medicine reports2018
High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Nitro-oleic acid activation of endothelial PPARγ signaling pathway alleviates neurovascular injury and improves functional outcomes in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2026Article
- Effects of High Glucose Concentrations on PC12 Cells: Possible Implications on Neurodegeneration.Current issues in molecular biology · 2025Article
- Endothelial peroxiredoxin-4 is indispensable for blood-brain barrier integrity and long-term functional recovery after ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Potential mechanism of the Shunaoxin pill for preventing cognitive impairment in type 2 diabetes mellitus.Frontiers in neurology · 2022Article
- Green tea protects against hippocampal neuronal apoptosis in diabetic encephalopathy by inhibiting JNK/MLCK signaling.Molecular medicine reports · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
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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