Abstract
Event Abstract Back to Event NF-kapaB rela-deficient macrophages fail to support bone formation and maintain the microenvironment for hematopoiesis after X-ray irradiation and HSC transplantation. Setsuko Mise-Omata1*, Taro Fukazawa1, Yuichi Obata1 and Takahiro S. Doi1 1 RIKEN Institute, BioResource Center, Japan In bone, cells derived from HSCs and MSCs are interacted each other. Bone is remodeled by osteoblasts derived from MSCs and osteoclasts from HSCs. The maintenance and differentiation of HSCs are supported by niche cells derived from MSC. NF-kappaB is an important transcription factor for hematopoiesis, bone remodeling, and inflammation. rela-/- fetal liver chimeric mice, which are prepared by transferring fetal liver cells into lethally irradiated host mice, are known to have reduced lymphopoiesis, although the hematopoietic activity of HSCs is intact. We found that they also developed osteoporosis. In rela-/- chimeric mice, bone formation was declined, but differentiation of osteoclasts was not enhanced. The most severe osteoporotic rela-/- chimeric mice possessed enhanced mobilization of HPCs in the peripheral, implying an impairment of microenvironment for hematopoiesis in rela-/- chimeric mice. Recently, macrophages in bone marrow are known to be important to maintain the microenvironment and to support bone formation. In order to assess the ability of F4/80+ macrophages to support bone formation, we co-transferred wild type F4/80+ macrophages with fetal liver cells into the host mice. As a result, the bone formation was rescued, indicating that a defect of rela-/- macrophages caused reduced bone formation. rela-/- macrophages more express NOS2, a typical M1 type inflammatory gene, but less express PGE2, important for wound healing and bone formation. The failure of wound healing after X-ray irradiation caused by a defect of macrophage function may occur, resulting in reduced bone formation and impairment of microenvironment for hematopoiesis in rela-/- chimeric mice. Keywords: Hematopoietic Stem Cells, NF-kB, osteoimmunology, Macrophages, Osteoporosis Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Mise-Omata S, Fukazawa T, Obata Y and Doi TS (2013). NF-kapaB rela-deficient macrophages fail to support bone formation and maintain the microenvironment for hematopoiesis after X-ray irradiation and HSC transplantation.. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00965 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 27 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Setsuko Mise-Omata, RIKEN Institute, BioResource Center, Tsukuba, Ibaraki, 3050074, Japan, smise@brc.riken.jp Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Setsuko Mise-Omata Taro Fukazawa Yuichi Obata Takahiro S Doi Google Setsuko Mise-Omata Taro Fukazawa Yuichi Obata Takahiro S Doi Google Scholar Setsuko Mise-Omata Taro Fukazawa Yuichi Obata Takahiro S Doi PubMed Setsuko Mise-Omata Taro Fukazawa Yuichi Obata Takahiro S Doi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
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