The role of G-protein-coupled receptor kinase 2 in diabetic mechanical hyperalgesia in rats.

Xiu-Hua Xu, Rui-Qin Du, Lin Li, Lin-Lin Yang, Yi Zhang, Quan-Min Li

European journal of pain (London, England) 2021 Oct

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Previous studies have indicated a negative correlation between GRK2 expression and pain development and transmission. Here, we investigated whether G-protein-coupled receptor kinase 2 (GRK2) was involved in regulating diabetic mechanical hyperalgesia (DMH). The adeno-associated viral vectors containing the GRK2 gene (AAV-GRK2) were used to up-regulate GRK2 protein expression. The expression of GRK2 and exchange protein directly activated by cyclic adenosine monophosphate 1 (Epac1) in the dorsal root ganglion (DRG) of lumbar 4-6 was detected via immunoblotting and immunohistochemistry, and the transfection of the GRK2 gene was detected by immunofluorescence. Low levels of GRK2 were able to sustain STZ-induced pain in DMH rats. Intrathecal injection of AAV-GRK2 vector up-regulated GRK2 expression, providing pain rain to rats with DMH. With an increase in DMH duration, there was a decrease in paw withdrawal threshold (PWT) value, aggravating the pain, resulting in a decreasing pattern in GRK2 protein expression over time, whereas Epac1 protein expression showed an opposite trend. GRK2 expression regulated DMH progression and is expected to play a role in the development of targeted therapy for DMH. GRK2 and Epac1 expressions play a vital role in maintaining pain in DMH rats. © 2021 European Pain Federation - EFIC®.

Citation

Xiu-Hua Xu, Rui-Qin Du, Lin Li, Lin-Lin Yang, Yi Zhang, Quan-Min Li. The role of G-protein-coupled receptor kinase 2 in diabetic mechanical hyperalgesia in rats. European journal of pain (London, England). 2021 Oct;25(9):2039-2049