Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 24, Issue 15, Pages 8650-8661Publisher
WILEY
DOI: 10.1111/jcmm.15496
Keywords
calcitonin; intervertebral disc degeneration; protein kinase C; rat caudal model
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Funding
- National Natural Science Foundation of China [81472132, 81572183, 81672220, 91849114]
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Intervertebral disc degeneration (IVDD) is the most critical factor that causes low back pain. Molecular biotherapy is a fundamental strategy for IVDD treatment. Calcitonin can promote the proliferation of chondrocytes, stimulate the synthesis of matrix and prevent cartilage degeneration. However, its effect and the underlying mechanism for IVDD have not been fully revealed. Chondrogenic specific matrix components' mRNA expression of nucleus pulposus cell (NPC) was determined by qPCR. Protein expression of NPC matrix components and protein kinase C was determined by Western blotting. A rat caudal intervertebral disc degeneration model was established and tested for calcitonin in vivo. IL-1 induced NPC change via decreasing protein kinase C (PKC)-epsilon phosphorylation, while increasing PKC-delta phosphorylation. Calcitonin treatment could prevent or reverse IL-1-induced cellular change on PKC signalling associated with degeneration. The positive effect of calcitonin on IVDD in vivo was verified on a rat caudal model. In summary, this study, for the first time, elucidated the important role of calcitonin in the regulation of matrix components in the nucleus of the intervertebral disc. Calcitonin can delay degeneration of the intervertebral disc nucleus by activating the PKC-epsilon pathway and inhibiting the PKC-delta pathway.
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