Bone marrow mesenchymal stem cells and TGF-β signaling in bone remodeling

被引：395

作者：

Crane, Janet L. ^{[1
,2
]}

Cao, Xu ^{[1
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Orthopaed Surg, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2014年 / 124卷 / 02期

关键词：

GROWTH-FACTOR-BETA; CAMURATI-ENGELMANN-DISEASE; LATENCY-ASSOCIATED PEPTIDE; DOMAIN-SPECIFIC MUTATIONS; PARATHYROID-HORMONE; TRANSFORMING GROWTH-FACTOR-BETA-1; FACTOR-I; OSTEOBLASTIC CELLS; ANABOLIC ACTIVITY; OXIDATIVE STRESS;

D O I：

10.1172/JCI70050

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

100103 [病原生物学]; 100218 [急诊医学];

摘要：

During bone resorption, abundant factors previously buried in the bone matrix are released into the bone marrow microenvironment, which results in recruitment and differentiation of bone marrow mesenchymal stem cells (MSCs) for subsequent bone formation, temporally and spatially coupling bone remodeling. Parathyroid hormone (PTH) orchestrates the signaling of many pathways that direct MSC fate. The spatiotemporal release and activation of matrix TGF-beta during osteoclast bone resorption recruits MSCs to bone-resorptive sites. Dysregulation of TGF-beta alters MSC fate, uncoupling bone remodeling and causing skeletal disorders. Modulation of TGF-beta or PTH signaling may reestablish coupled bone remodeling and be a potential therapy.

引用

页码：466 / 472

页数：7

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