연구논문

세부과제번호 2014M3A9D5A01073658 단계 2단계 2차년도
세부과제명 마우스 골격계 표현형분석을 통한 골질환 진단 및 골격계 질환 분석 공동 유/무 Y
SCI여부 Y 게재년월 -
논문제목 The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages.
총저자명 Daejin Lim, Kwang Soo Kim, Jae-Ho Jeong, Oriana Marques, Hyun-Ju Kim, Miryoung Song, Tae-Hoon Lee, Jae Il Kim, Hueng-Sik Choi, Jung-Joon Min, Dirk Bumann, Martina U Muckenthaler, Hyon E Choy
학술지명 Nat Commun 게재권(호) 9(1)
저널구분 - 페이지수 2091
참여연구원 - 연구책임자 최제용
과제기여도 10 PMID 29844422
사사기관수 - IF (년도) 12.353
제1저자 Daejin Lim 교신저자 Hyon E Choy
공동저자 Kwang Soo Kim, Jae-Ho Jeong, Oriana Marques, Hyun-Ju Kim, Miryoung Song, Tae-Hoon Lee, Jae Il Kim, Hueng-Sik Choi, Jung-Joon Min, Dirk Bumann, Martina U Muckenthaler
초록
Macrophages release iron into the bloodstream via a membrane-bound iron export protein, ferroportin (FPN). The hepatic iron-regulatory hormone hepcidin controls FPN internalization and degradation in response to bacterial infection. Salmonella typhimurium can invade macrophages and proliferate in the Salmonella-containing vacuole (SCV). Hepcidin is reported to increase the mortality of Salmonella-infected animals by increasing the bacterial load in macrophages. Here we assess the iron levels and find that hepcidin increases iron content in the cytosol but decreases it in the SCV through FPN on the SCV membrane. Loss-of-FPN from the SCV via the action of hepcidin impairs the generation of bactericidal reactive oxygen species (ROS) as the iron content decreases. We conclude that FPN is required to provide sufficient iron to the SCV, where iron serves as a cofactor for the generation of antimicrobial ROS rather than as a nutrient for Salmonella.
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