报告题目：Rethinking Bone Biology: Targeting skeletal endothelium to promote osteogenesis

报告人：Dr. Ren Xu (许韧), from Weill Cornell Medicine, Cornell University 

主持人：罗剑 教授

报告时间：2018年5月7日 14:00-15:00 （周一）

报告地点：生命科学学院534小会议室

举办单位：生命科学学院/科技处

 

报告人简介：Dr. Ren Xu 2005年本科毕业于安徽师范大学，2008年在厦门大学获得硕士学位，2013年在东京医科和牙科大学获得博士学位。目前是美国康奈尔大学医学院博士后。许博士一直从事骨质疏松的调控机制研究，已作为第一作者在国际知名学术期刊Nature, Nat Med等杂志上发表论文多篇，获得多个国际骨科学会青年科学家奖。

 

报告摘要：Recent studies have identified a specialized subset of CD31hiEMCNhi vascular endothelium that positively regulates bone formation. However, it remains unclear how CD31hiEMCNhi endothelium levels are coupled to anabolic bone formation. Mice with an osteoblast-specific deletion of Schnurri-3 (Shn3), which have markedly elevated bone formation, demonstrated an increase in CD31hiEMCNhi endothelium. Transcriptomic analysis identified SLIT3 as an osteoblast-derived, SHN3-regulated proangiogenic factor. Genetic deletion of Slit3 reduced skeletal CD31hiEMCNhi endothelium, resulted in low bone mass due to impaired bone formation and partially reversed the high bone mass phenotype of Shn3-/- mice. This coupling between osteoblasts and CD31hiEMCNhi endothelium is essential for bone healing, as shown by defective fracture repair in SLIT3-mutant mice and enhanced fracture repair in SHN3-mutant mice. Finally, administration of recombinant SLIT3 both enhanced bone-fracture healing and counteracted bone loss in a mouse model of postmenopausal osteoporosis. Thus, drugs that target the SLIT3 pathway may represent a new approach for vascular-targeted osteoanabolic therapy to treat bone loss.