刘凤珍
Macrophage exosomes modified by miR-365-2-5p promote osteoblast bone formation by targeting OLFML1
报告人:刘凤珍
所在单位:山东第一医科大学附属聊城医院
报告人简介:
刘凤珍，博士，研究员，硕导，现任山东第一医科大学附属聊城医院/山东省聊城市人民医院科研处副主任、山东省聊城市生物材料学重点实验室主任。中国科学院大学博士，清华大学博士后，哈佛大学医学院全球医疗管理青年攀登人才计划，国家留学基金委资助美国哥伦比亚大学医学院访问学者，中国科协科普专家、山东省高层次人才，山东省工信厅专家库聘任专家。兼任BEBT国际会议分会主席、American Association for Science and Technology Life Membership（AASCIT委员）、中国微循环学会转化医学专委会常委、中华口腔医学会口腔材料专业委员会委员、中华医学会医学工程学分会干细胞工程学组委员、山东省医院协会科研管理分会常务委员等。主要从事生物医用材料产品的研发及临床转化。发表 SCI 50 余篇，中文 5 篇，专利 3 项，主编中英文著作 3 部。承担及参与国家重点研发计划项目、国家自然基金、博士后基金、山东省自然基金等省部级以上项目 10 余项。获山东省医学科技奖、山东省高校自然科学奖等 6 项。联合培养博士 5 名，其中 1 名博士获山东大学优秀毕业生。多次应邀国际国内会议作学术报告。
报告摘要:
In the bone immune microenvironment, immune cells can regulate osteoblasts through a complex communication network. Macrophages are core cells that mediate immune osteogenesis,exosomes derived from them have osteogenic regulation and can be used as carriers in bone tissue engineering. However, there are problems with exosomal therapy alone, such as poor targeting, and the content of loaded molecules cannot reach the therapeutic concentration. In this study, macrophage-derived exosomes modified with miR-365-2-5p were developed to accelerate bone healing. MC3T3-E1 cells were incubated with the culture supernatants of M0, M1 and M2 macrophages, and it was found that the culture medium of M2 macrophages had the most significant effects in contributing to osteogenesis. High-throughput sequencing identified that miR-365-2-5p was significantly expressed in exosomes derived from M2 macrophages. We incubated MC3T3-E1 with exosomes overexpressing or knocking down miR-365-2-5p to examine the biological function of exosome miR-365-2-5p on MC3T3-E1 differentiation. The findings suggest that miR-365-2-5p secreted by exosomes increased the osteogenesis of MC3T3-E1. Moreover, miR-365-2-5p had a direct influence over osteogenesis for MC3T3-E1. Sequencing analysis combined with dual luciferase detection indicated that miR-365-2-5p binded to the 3'UTR of OLFML1. In summary, exosomes secreted by M2 macrophages targeted OLFML1 through miR-365-2-5p to facilitate osteogenesis.
