Prior research efforts have demonstrated a link between neuroinflammation and the progression of Painful Diabetic Neuropathy (PDN), a chronic cascade of nerve damage that presents as tingling, numbness, hypersensitivity to touch, or intense pain. Current treatments are focused on pain management, serving to temporarily mask these symptoms without repressing or slowing nerve damage. The chemokine-receptor system has been closely studied for its role in perpetuating neuropathic pain, although its precise mechanistic involvement remains unclear due to the network’s complexity. Because of its likely role in regulating neuropathic pain, targeting CCR2 may be the key to effective treatment of PDN.
Alternative splicing of CCR2 leads to two distinct isoforms with different C-terminus sequences, CCR2A and CCR2B. The present study was intended to differentiate between these isoforms through specific primer design, selection of optimized pairs, RT-PCR, and amplicon sequencing to verify the PCR products. However, the study has revealed a third, previously unreported isoform, CCR2C, due to evidence of alternative splicing and both the absence and insertion of parts of A and B. In the long term, we predict that the relationship between CCR2’s alternatively spliced transcript variants will lead to a distinct pattern of isoform prevalence in individuals suffering from PDN. Discerning the genetic profiles of patients with PDN and healthy individuals will clarify the complex mechanism driving CCR2’s intracellular interactions and offer more effective therapeutic options.
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Copyright (c) 2021 Justine Soltys, Lei Yu