Inhibition of Axinl in osteoblast precursor cells leads to defects in postnatal bone growth through suppressing osteoclast formation

查看全文 作　　者：Bing [1,2,3]Shu;Yongjian [1,2,3]Zhao;Shitian [1,2,3]Zhao;Haobo [4]Pan;Rong [5]Xie;Dan [4]Yi;Ke [5]Lu;Junjie [1,2,3]Yang;Chunchun [1,2,3]Xue;Jian Huang Jing [1,3]Wang;Dongfeng [1,2,3]Zhao;Guozhi [6]Xiao;Yongjun [1,2,3]Wang;Di [4]Chen

机构地区：[1]Longhua Hospital,Shanghai University of Traditional Chinese Medicine,725 WanPing South Road,Shanghai 200032,China;[2]Spine Institute,Shanghai Academy of Traditional Chinese Medicine,725 WanPing South Road,Shanghai 200032,China;[3]Key Laboratory,Ministry of Education of China,725 WanPing South Road,Shanghai 200032,China;[4]Research Center for Human Tissues and Organs Degeneration,Shenzhen Institutes of Advanced Technology,Chinese Academy of Sciences,Shenzhen 518055,China;[5]Department of Orthopedic Surgery,Rush University Medical Center,Chicago,IL 60612,USA;[6]School of Medicine,Southern University of Science and Technology,Shenzhen 518055,China

出　　处：《Bone Research》索引2020年第8卷第3期,共8页

基　　金：National Natural Science Foundation of China(NSFC)(81973876,81673991 to BS,81730107 to YJW and 81603643 to YJZ);The National Key R&D Program of China(2018YFC1704302 to YJW);The Program for Innovative Research Team in University,Ministry of Education of China(IRT1270 to YJW);The Program for Innovative Research Team,Ministry of Science and Technology of China(2015RA4002 to YJW);The Three Years Action to Accelerate the Development of Traditional Chinese Medicine Plan(ZY(2018-2020)-CCCX-3003 to YJW);National Natural Science Foundation of China(NSFC)(81672227)and a Frontier Science of CAS grant(QYZDB-SSW-JSC030)to HP.National Natural Science Foundation of China(NSFC)(81991513)to GX. 摘　　要：Axinl is a negative regulator of β-catenin signaling and its role in osteoblast precursor cells remains undefined.In the present studies,we determined changes in postnatal bone growth by deletion of Axinl in osteoblast precursor cells and analyzed bone growth in newborn and postnatal Axin1 O5X mice and found that hypertrophic cartilage area was largely expanded in AxinlOSX KO mice.A larger number of chondrocytes and unabsorbed cartilage matrix were found in the bone marrow cavity of Axin1OSX KO mice.Osteoclast formation in metaphyseal and subchondral bone areas was significantly decreased,demonstrated by decreased TRAPpositive cell numbers,associated with reduction of MMP9-and cathepsin K-positive cell numbers in Axin1 O5X KO mice.OPG expression and the ratio of O p g to Rankl were significantly increased in osteoblasts of Axinl O5X KO mice.Osteoclast formation in primary bone marrow derived microphage(BMM)cells was significantly decreased when BMM cells were cultured with conditioned media(CM)collected from osteoblasts derived from Axin1OSX mice compared with BMM cells cultured with CM derived from WT mice.Thus,the loss of Axinl in osteoblast precursor cells caused increased OPG and the decrease in osteoclast formation,leading to delayed bone growth in postnatal Axin1°sx KO mice. 关键词：AXIN OSTEOCLAST CAVITY

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Inhibition of Axinl in osteoblast precursor cells leads to defects in postnatal bone growth through suppressing osteoclast formation

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