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논문 기본 정보

자료유형
학술저널
저자정보
Feng Wang (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Hong Sung Min (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Haojie Shan (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Fuli Yin (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Chaolai Jiang (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Yang Zong (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Xin Ma (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Yiwei Lin (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Zubin Zhou (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital) Xiaowei Yu (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital)
저널정보
대한면역학회 Immune Network Immune Network Vol.22 No.3
발행연도
2022.6
수록면
71 - 81 (11page)

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IL-34 can promote osteoclast differentiation and activation, which may contribute to steroid-induced osteonecrosis of the femoral head (ONFH). Animal model was constructed in both BALB/c and IL-34 deficient mice to detect the relative expression of inflammation cytokines. Micro-CT was utilized to reveal the internal structure. In vitro differentiated osteoclast was induced by culturing bone marrow-derived macrophages with IL-34 conditioned medium or M-CSF. The relative expression of pro-inflammation cytokines, osteoclast marker genes, and relevant pathways molecules was detected with quantitative real-time RT-PCR, ELISA, and Western blot. Up-regulated IL-34 expression could be detected in the serum of ONFH patients and femoral heads of ONFH mice. IL-34 deficient mice showed the resistance to ONFH induction with the up-regulated trabecular number, trabecular thickness, bone value fraction, and down-regulated trabecular separation. On the other hand, inflammatory cytokines, such as TNF-α, IFN-γ, IL-6, IL-12, IL-2, and IL-17A, showed diminished expression in IL-34 deficient ONFH induced mice. IL-34 alone or works in coordination with M-CSF to promote osteoclastogenesis and activate ERK, STAT3, and non-canonical NF-κB pathways. These data demonstrate that IL-34 can promote the differentiation of osteoclast through ERK, STAT3, and non-canonical NF-κB pathways to aggravate steroid-induced ONFH, and IL-34 can be considered as a treatment target.

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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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