ArticleMolecular genetics & genomic medicine2019
Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 3 citations in OpenAlex.
- Selective inhibition of monoamine oxidase B represents a therapeutic strategy for diabetic peripheral neuropathy.Acta pharmacologica Sinica · 2026Article
- PPM1A dysfunction aggravates DPN pathology through NF-κB/NLRP3/p-tau axis involving Schwann cell/DRG neuron crosstalk.Journal of translational medicine · 2026Article
- Glabridin as a selective Kv2.1 inhibitor ameliorates DPN pathology by disrupting the Aβ/Kv2.1/JNK/NF-κB/NLRP3/p-Tau pathway.Acta pharmacologica Sinica · 2025Article
- Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia.Molecular genetics & genomic medicine · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveWe analyzed the function of Tau protein to explore the underlying mechanism of axonal transport disorder caused by persistent pressure in the dorsal root ganglia (DRG).
methodsWistar rats were divided into the sham operated group, the control group and the experimental group. The Wistar rat model of continuous compression of DRG was used for further investigation. DRG neurons were extracted and cultured, and the protein content was detected using bicinchoninic acid method. Western blotting and immunofluorescence assays were performed to detect the protein content. Intraperitoneal injection of lithium chloride was performed for interaction with Tau. The results were then analyzed statistically.
resultsAfter 2 weeks of sustained pressure, the expression level of Tau
conclusionChronic compression of DRG and hypoxia caused phosphorylation of Tau in axons and inhibition of PSD-95, and the function of the synaptic glutamic acid vesicle is defective in the synapse. This process is crucial in the development and progression of axonal transport dysfunction induced by chronic DRG compression, and phosphorylation of Tau plays a substantial role in this process.
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