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RISS 인기검색어
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- 저자 : 정연관 ( Youn Kwan Jung ) (검색결과 2 건)
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정연관 ( Youn Kwan Jung ),박혜리 ( Hye Ri Park ),이은주 ( Eun Ju Lee ),정동형 ( Dong Hyoung Jeong ),김건우 ( Gun Woo Kim ),최제용 ( Je Yong Choi ),한승우 ( Seung Woo Han ) 대한류마티스학회 2012 대한류마티스학회지 Vol.19 No.4
DICAM, a dual Ig domain containing adhesion molecule, is involved in cell-cell adhesion through direct interaction with αvβ3 integrin. In our previous study showing the inhibitory role of DICAM in osteoclast differentiation, we found that DICAM also has a suppressive role in macrophage, the precursor cell of osteoclast, The role of DICAM in macrophage activation at the inflammatory milieu, however, remains obscure, Methods, Expression pattern of DICAM by inflammatory cytokines and lipopolysaccharide (LPS) was studied with RAW264.7, a murine macrophage cell line, To study the role of DICAM on macrophage activation, we stably transduced DICAM, or empty vector, into RAW264.7, and then compared the LPS-mediated activation such as spreading and TNF-a production, Results, DICAM was abundantly expressed in the synovial tissue of collagen-induced arthritis. When we assessed the expression of DICAM in RAW264.7 cells by mediators of inflammation, inflammatory cytokines, such as TNF-α, IL-1β, and IFN-γ, and M-CSF increased the expression of DICAM; however, LPS decreased. Functionally, DICAM that stably transduced-RAW264.7 cells showed attenuation of LPS-mediated macrophage activation including spreading and TNF-α production. DICAM decreased the phosphorylation of JNK MAP kinase by M-CSF and LPS stimulation, which was corroborated by a decrease in the expression of ITAM-associated receptors including Trem2, Pira1, and Oscar. Finally, a recombinant ectodomain of DICAM suppressed LPS-induced activation of RAW264.7 cells, Conclusion. These results indicate that DICAM acts as a negative regulator of LPS-mediated macrophage activation.
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THP-1 세포주의 대식세포 분화과정에서 DICAM에 의한 제 1형 인터페론 시스템의 억제
김보연 ( Bo Yeon Kim ),박인 ( In Park ),정연관 ( Youn Kwan Jung ),한민수 ( Min Su Han ),김건우 ( Gun Woo Kim ),한승우 ( Seung Woo Han ) 대한류마티스학회 2014 대한류마티스학회지 Vol.21 No.3
Objective. We have previously shown that DICAM inhibits LPS-mediated macrophage differentiation. However, less is known about the exact action mechanisms of DICAM on the macrophage function and differentiation. Methods. To induce differentiation into a resting M0 macrophage, THP-1 cells were cultured with 100 nM PMA for 24 h, and then rested for 3 days. THP-1 cells were infected with 50 moi of control LacZ- or DICAM-containing adenovirus. The RNA expression profile associated with DICAM during THP-1 differentiation was analyzed with a microarray chip and in silico analysis with Ingenuity Pathway Analysis (IPA) program. Results. A disease and function analysis of the microarray data in DICAM-overexpressed THP-1 cells revealed a suppression in the expression of multiple genes involved in the response of myeloid cells and phagocytes, and an increase of genes associated with apoptosis of fibroblast cell-line, and viral infection and replication. The canonical pathway analysis also showed the most prominent changes of signaling pathways that involve inflammation responses. An upstream regulator analysis identifyingmolecules upstream of the genes that potentially explain the observed expression changes revealed that IRF7 and the genes in type 1 interferon system, such as IFNA2 and IFNAR,was significantly attenuated by DICAM. A mechanistic network analysis confirmed a direct causal association between IRF7 and type 1 interferon system. A real-time RT-PCR analysis validating the microarray data verified the significant suppression of IRFs, IFNA2, and IFNB1. Conclusion. These results suggest that DICAM can be a critical regulator of type 1 interferon system, which is an essential mediator in the process of intracellular infection and systemic lupus erythematosus.
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