연구단계 | 1단계 :1년차 | ||
논문제목(영문) | Mesenchymal stem cells reciprocally regulate the M1/M2 balance in mouse bone marrow-derived macrophages. | ||
국내외구분 | 국외 | SCI여부 | SCI |
연구책임자역활 | 교신저자 | 논문기여율 | 30% |
주저자명 | Cho DI | ||
교신저자명 | Ahn Y | ||
공동저자명 | Kim MR, Jeong HY, Jeong HC, Jeong MH, Yoon SH, Kim YS | ||
게제년월일 | 2014-01-10 | ||
ISSN | 1226-3613 | ||
Impact Factor | 2.462 | ||
학술지명 | Exp Mol Med | ||
서지사항 | 0집 / 46권 / 0호, 페이지(e70 - e70) | ||
병기표기 | 단독 | ||
Acknowledgement 기재여부 |
예
※ Acknowledgement가 기재된 논문만 연구과제의 성과로 인정. - 국문 표기 : "본 연구는 보건복지부 보건의료연구개발사업의 지원에 의하여 이루어진 것임. (HI13C1527)" - 영문 표기 : "This study was supported by a grant of the Korean Health Technology R&D Project, (HI13C1527) Ministry of Health & Welfare, Republic of Korea. " |
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요약초록문 (Abstract) 입력 |
Mesenchymal stem cells (MSCs) have been widely studied for their applications in stem cell-based regeneration. During myocardial infarction (MI), infiltrated macrophages have pivotal roles in inflammation, angiogenesis and cardiac remodeling. We hypothesized that MSCs may modulate the immunologic environment to accelerate regeneration. This study was designed to assess the functional relationship between the macrophage phenotype and MSCs. MSCs isolated from bone marrow and bone marrow-derived macrophages (BMDMs) underwent differentiation induced by macrophage colony-stimulating factor. To determine the macrophage phenotype, classical M1 markers and alternative M2 markers were analyzed with or without co-culturing with MSCs in a transwell system. For animal studies, MI was induced by the ligation of the rat coronary artery. MSCs were injected within the infarct myocardium, and we analyzed the phenotype of the infiltrated macrophages by immunostaining. In the MSC-injected myocardium, the macrophages adjacent to the MSCs showed strong expression of arginase-1 (Arg1), an M2 marker. In BMDMs co-cultured with MSCs, the M1 markers such as interleukin-6 (IL-6), IL-1β, monocyte chemoattractant protein-1 and inducible nitric oxide synthase (iNOS) were significantly reduced. In contrast, the M2 markers such as IL-10, IL-4, CD206 and Arg1 were markedly increased by co-culturing with MSCs. Specifically, the ratio of iNOS to Arg1 in BMDMs was notably downregulated by co-culturing with MSCs. These results suggest that the preferential shift of the macrophage phenotype from M1 to M2 may be related to the immune-modulating characteristics of MSCs that contribute to cardiac repair. |
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