Release date: 2018-03-28
Today, another Chinese scholar's research has been published on the cover of a well-known academic journal. Professor Xin Wenjun from Zhongshan Medical College of Sun Yat-sen University published a paper in the latest issue of Science Signaling, introducing a chronic pain. The signaling pathway and clarify the key biological mechanisms behind it. This research is expected to bring a new pain relief program.
The research of Professor Xin Wenjun's team is on the cover of Science Signaling (Source: Science Signaling)
Professor Wen Wenjun's main research direction is the plasticity of synapses and the pathophysiology of pain. We know that the perception of pain is closely related to the synaptic activity of neurons. If these neurons are overexcited, it will cause chronic pain, but the specific biological mechanism behind it is not well clarified.
In this study, the “All-China Team†team first focused on a classic finding in the field of pain – the anticancer drug oxaliplatin caused significant pain perception abnormalities. Since the palmitoylation modification of the δ-catenin protein is associated with synaptic plasticity in pain-related neurons, the researchers naturally linked the two. Is oxaliplatin a side effect of abnormal pain caused by protein modification? The results support this: under the action of oxaliplatin, the palmitoylation modification of brain DRG neurons is significantly increased; by inhibiting this protein modification, we can also reduce the abnormal pain caused by oxaliplatin. These results indicate that the palmitoylation modification of the delta-catenin protein is essential for the perception of pain.
As a common post-translational protein modification, palmitoylation increases the hydrophobicity of the protein and helps the protein "exchange" with the lipid bilayer. While δ-catenin is a cell adhesion protein, it is more structurally active. There are some key links between it and pain perception. To find the last few puzzles, the researchers did a screening to examine the relationship between δ-catenin and Nav (sodium-gated-gated channels), which are involved in mediating the action potentials of pain-related neurons. Using co-immunoprecipitation, the researchers found that δ-catenin binds mainly to Nav1.6 and Nav1.7, whereas Nav1.6 binds to palmitoylation. This time, the palmitoylation and pain perception are brought together.
Under normal circumstances, Nav1.6 is mainly present in the cytoplasm. And when it needs to work, it is transported to the cell surface of the neuron. Acts as a channel for sodium ions. Researchers have also boldly speculated that at least one protein involved in intracellular transport will bind to δ-catenin. Also using the method of co-immunoprecipitation, the two kinesins, KIF3A and KIF3B, stood out and showed the ability to bind to δ-catenin.
Remember the oxaliplatin mentioned above? It has side effects that cause abnormal pain. In mice, oxaliplatin significantly increased the binding of δ-catenin to KIF3A, suggesting that KIF3A plays a major role. Further studies have shown that in mice with neuropathic pain, palmitoylation of δ-catenin does promote the binding of KIF3A and Nav1.6 in key neurons and allows the three proteins to form a complex.
Palmitoylation of δ-catenin promotes the formation of protein complexes (Source: Science Signaling)
The researchers believe that this protein complex may increase the level of Nav1.6 on the surface of neuronal cell membranes with the help of δ-catenin and KIF3A, making neurons more sensitive to pain. Considering the large number of patients living in chronic pain, Science Signaling's short review suggests that this research is expected to bring new drug-making targets for the benefit of humanity.
We once again congratulate Professor Xin Wenjun's team on the research of "Science Signaling" cover, and look forward to seeing more outstanding research from Chinese scholars in the future!
References: [1] Palmitoylation of δ-catenin promotes kinesin-mediated membrane trafficking of Nav1.6 in sensory neurons to promote neuropathic pain
Source: Academic Jingwei
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