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Del-1, an Endogenous Inhibitor of TGF-β Activation, Attenuates Fibrosis
  • 작성일2021-02-22
  • 최종수정일2021-02-22
  • 담당부서연구기획과
  • 연락처043-719-8033
  • 조회수237

Frontiers in Immunology, 2020.11, 68-0, DOI: https://doi.org/10.3389/fimmu.2020.00068


Del-1, an Endogenous Inhibitor of TGF-β Activation, Attenuates Fibrosis

Kim DY, Lee SH;Fu Y;Jing F;Kim WY;Hong SB;Song JA;Choe H;Ryu H;Kim M;Lim D;Kim MS;Yun CO;Lee T;Hyun H;Choi E


Abstract

    Uncontrolled activation of transforming growth factor (TGF)-b results in a wide range of pathologic conditions. Therapeutic interventions to regulate TGF-b signaling during fibrosis have been developed but the effectiveness is still limited. Here, we show that developmental endothelial locus-1 (Del-1) ameliorates fibrosis in mice by inhibiting av integrin-mediated activation of TGF-b. Del-1 bound to avb6 integrin, an important activator of TGF-b, and inhibited the binding of avb6 integrin to the latency-associated peptide (LAP), thereby suppressing av integrin-mediated activation of TGF-b. Lack of Del-1 increased colocalization of av integrin and LAP in the lungs, which was reversed by Del-1 supplementation. The crucial role of Del-1 in regulating TGF-b activity was recapitulated in a mouse model of fibrosis using an adenovirus expressing inactive TGF-b1. Del-1 supplementation improved the pathological characteristics of the mice and reduced mortality. Thus, we propose that Del-1 is a negative regulator of TGF-b activation and a potential anti-fibrotic factor.



  • 본 연구는 질병관리본부 연구개발과제연구비를 지원받아 수행되었습니다.
  • This research was supported by a fund by Research of Korea Centers for Disease Control and Prevention.


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