The role of G-protein-coupled receptor kinase 2 in diabetic mechanical hyperalgesia in rats
| Autor: | Quan-Min Li, Yi Zhang, Li Lin, Lin-Lin Yang, Xiu-Hua Xu, Rui-Qin Du |
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| Rok vydání: | 2020 |
| Předmět: |
endocrine system
medicine.medical_specialty G-Protein-Coupled Receptor Kinase 2 Pain chemistry.chemical_compound Dorsal root ganglion Downregulation and upregulation Internal medicine Ganglia Spinal medicine Diabetes Mellitus Animals Cyclic adenosine monophosphate Receptor G protein-coupled receptor kinase biology Chemistry Kinase Beta adrenergic receptor kinase Transfection Rats Anesthesiology and Pain Medicine Endocrinology medicine.anatomical_structure Hyperalgesia biology.protein |
| Zdroj: | European journal of pain (London, England)REFERENCES. 25(9) |
| ISSN: | 1532-2149 |
| Popis: | Background 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). Methods The adeno-associated viral vectors containing the GRK2 gene (AAV-GRK2) were used to upregulate 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. Results Low levels of GRK2 were able to sustain STZ-induced pain in DMH rats. Intrathecal injection of AAV-GRK2 vector upregulated 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. Conclusion 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. |
| Databáze: | OpenAIRE |
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