Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia

Abstract

Objective We 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). Methods Wistar 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. Results After 2 weeks of sustained pressure, the expression level of Tau396 increased by 33%, while Tau404 increased by 25% in the DRG of the experimental group (p < 0.05). The expression level of PSD‐95 in the DRG decreased by 15% (p < 0.05), while the expression of vGluT1, vGluT3 and vAchT decreased significantly in the DRG of the experimental group (p < 0.05). There was no significant difference in the expression of vGluT2 and vGAT among the three groups (p > 0.05). After intervention with lithium chloride, the expression of phosphorylated Tau at the above sites decreased in varying degrees compared with the model group. The expression level of Tau404 was reduced by 55%, and that of Tau199 by 60% in the DRG of the experimental group. Conclusion Chronic 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.

Scoping review and interpretation of Myofascial Pain/Fibromyalgia syndrome: an attempt to assemble a medical puzzle

“…A reader adopting this "biological ethos" should not be surprised, for example, by a study finding that fibromyalgia patients have elevated serum tau and amyloid beta levels, since studies suggest amyloid beta and the cytoskeletal protein tau and are affected by, or compensate for, mechanical stress. [221][222][223][224][225][226][227][228] At least we might want to exclude an organic fascial cause before perceiving these cases as psycho-functional disorders, even if the mechanism is still unclear, and even if it involves a degree of central sensitization. Is there enough empirical evidence to recognize MPS and fibromyalgia as honorable organic diseases, like any other, rather than psychosomatic?…”