Vitamin D Inhibits Activities of Metalloproteinase-9/-13 in Articular Cartilage In Vivo and In Vitro

• DOI: 10.3177/jnsv.65.107
• Publication Date: 2019-04-29T22:07:35Z
• Authors: Siwei LI; Guodong NIU; X. Neil DONG; Zhongjun LIU; Chunli SONG; Huijie LENG
• Keywords: Cartilage, Articular; Tumor Necrosis Factor-alpha; Matrix Metalloproteinase Inhibitors; Rats; Rats, Sprague-Dawley; 03 medical and health sciences; Chondrocytes; 0302 clinical medicine; Matrix Metalloproteinase 9; Matrix Metalloproteinase 13; Animals; Tetradecanoylphorbol Acetate; Female; Vitamin D

Low levels of serum vitamin D have been shown to accelerate progression of osteoarthritis. However, the role of vitamin D in articular cartilage degradation and osteoarthritis development is still unclear. This study investigated the effects of vitamin D on articular cartilage degradation by testing matrix metalloproteinase (MMPs) activities in articular cartilage using the rat vitamin D deficiency model at the animal level and rat articular chondrocytes at the cell level. The in vivo study showed vitamin D deficiency increased the expressions of MMP-9 and MMP-13 in rat articular cartilage, and the increase was inhibited by 1α,25(OH)2D3 supplementation. The increased production of MMP-9 and MMP-13 in the articular chondrocytes induced by tumor necrosis factor-α (TNF-α) or phorbol-12-myristate-13-acetate (PMA) was significantly suppressed by concomitant treatment with 1α,25(OH)2D3 in vitro. The increased level of C-telopeptide of type II collagen (CTX-II) induced by TNF-α or PMA was also significantly suppressed by concomitant treatment with 1α,25(OH)2D3 in vitro. Thus, vitamin D intake may inhibit MMP activities and take part in the process of articular cartilage degeneration and osteoarthritis progression.