Session Information
Date: Tuesday, November 10, 2015
Title: Biology and Pathology of Bone and Joint: Bone Remodeling and Metabolism
Session Type: ACR Poster Session C
Session Time: 9:00AM-11:00AM
Background/Purpose:
Interleukin-32 (IL-32) has been known to be implicated in the pathogenesis of various inflammatory diseases. Osteoporosis, characterized by low bone density and increases the risk of fracture, was prevalent in systemic inflammatory diseases mediated through the link between chronic inflammation and bone loss. In this study, we try to investigate the effects of IL-32γ in osteoporosis since the role of IL-32 in bone formation as well as bone resorption remains largely unknown.
Methods:
To determine whether IL-32γ affects bone formation, we examined bone volume of transgenic (TG) mice overexpressing IL-32γ by using micro-CT. Ovariectomized mice were used to know the effects of IL-32γ on osteoporosis in vivo. In addition, bone formation rate was evaluated by labeling with calcein, a marker of newly formed bone. To elucidate the mechanism of IL-32γ effect on bone metabolism, we measured the levels of Dickkopf-1 (DKK-1), is well-known as having an inhibitory effects on osteoblastogenesis. Further, the concentration of IL-32γ was measured in the peripheral blood from patients with osteoporosis.
Results:
Micro-CT analysis revealed that IL-32γ TG mice had an increased bone volume compared with wild-type (WT) mice. Furthermore, bone loss induced by ovariectomy was substantially attenuated in IL-32γ TG mice compared with that in WT mice. Importantly, IL-32γ TG mice had higher bone formation rate as assessed by the mineral apposition rate compared with WT mice. In addition, the level of DKK-1 was significantly lower in the IL-32γ TG mice than WT mice. Finally, we found that the concentration of IL-32γ was significantly lower in the blood of patients with osteoporosis than in those of healthy individuals.
Conclusion:
Our present study suggested that IL-32γ enhances bone formation through association with the decrease of DKK-1, which contributes to the protective effects on osteoporosis.
To cite this abstract in AMA style:
Hong S, Lee EJ, Kim SM, Chang EJ, Lim DH, Ghang B, Seo W, Kim YG, Lee CK, Yoo B. Interleukin-32γ Exhibited Protective Effects on Osteoporosis [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/interleukin-32i%c2%b3-exhibited-protective-effects-on-osteoporosis/. Accessed .« Back to 2015 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/interleukin-32i%c2%b3-exhibited-protective-effects-on-osteoporosis/