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Abstract
Background: Some reports have shown that metabolic syndrome, including hypertension, hyperlipidemia, and diabetes mellitus, contributes to osteoarthritis (OA) development. Further, lectin-like oxidized low-density lipoprotein (ox-LDL) and ox-LDL receptor-1 (LOX-1), which contributes to atherosclerosis, have also been considered factors contributing to OA development. Several studies have suggested that the LOX-1/ox-LDL system is involved in OA development in vitro. We have suggested the same and conducted in vitro and in vivo studies to validate this concept. However, the role of the LOX-1/ox-LDL system in OA development has not been clarified. This study aimed to identify the mechanism of the LOX-1/ox-LDL system to clarify OA development. Methods: A zymosan-induced arthritis model was used to identify the mechanism of the LOX-1/ox-LDL system using LOX-1-knockout (KO) mice. Zymosan was administered via the intra-articular route to induce arthritis. Results: From our experiment, we found that the LOX-1/ox-LDL system contributes to OA development through matrix metalloproteinase-3. Conclusion: Our findings suggest that the treatment of abnormal lipid metabolism may contribute to the prevention and suppression of arthritis.
Highlights
Osteoarthritis (OA), which is characterized by wear and tear of the articular cartilage, was previously believed to be caused by mechanical stress[1]
Our findings suggest that the treatment of abnormal lipid metabolism may contribute to the prevention and suppression of arthritis
Immunohistochemical staining revealed low-density lipoprotein (LDL) receptor-1 (LOX-1) and oxidized low-density lipoprotein (ox-LDL) expression in the chondrocytes and inflammatory synovial cells in WT mice (Figures 3, 4) but not in LOX-1 KO mice. These findings suggest that LOX-1/ox-LDL in the chondrocytes and inflammatory synovial cells are involved in the development of arthritis
Summary
Osteoarthritis (OA), which is characterized by wear and tear of the articular cartilage, was previously believed to be caused by mechanical stress[1]. Recent studies have suggested the role of other systemic factors[2]. One of them is metabolic syndrome[3, 4], including hypertension, hyperlipidemia, and diabetes mellitus, all of which lead to atherosclerosis[5]. Sawamura et al have reported that lectin-like, oxidized low-density lipoprotein (ox-LDL) and ox-LDL receptor-1 (LOX-1) contribute to atherosclerosis[7]. Some reports have shown that metabolic syndrome, including hypertension, hyperlipidemia, and diabetes mellitus, contributes to osteoarthritis (OA) development. Lectin-like oxidized low-density lipoprotein (ox-LDL) and ox-LDL receptor-1 (LOX-1), which contributes to atherosclerosis, have been considered factors contributing to OA development. Several studies have suggested that the LOX-1/ox-LDL system is involved in OA development in vitro. This study aimed to identify the mechanism of the LOX-1/ox-LDL system to clarify OA development
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