Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States of America.
Department of Biochemistry & Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America.
PLoS One. 2019 Jan 4;14(1):e0204197. doi: 10.1371/journal.pone.0204197. eCollection 2019.
Bone remodeling involves the coordinated actions of osteoclasts, which resorb the calcified bony matrix, and osteoblasts, which refill erosion pits created by osteoclasts to restore skeletal integrity and adapt to changes in mechanical load. Osteoblasts are derived from pluripotent mesenchymal stem cell precursors, which undergo differentiation under the influence of a host of local and environmental cues. To characterize the autocrine/paracrine signaling networks associated with osteoblast maturation and function, we performed gene network analysis using complementary "agnostic" DNA microarray and "targeted" NanoString nCounter datasets derived from murine MC3T3-E1 cells induced to undergo synchronized osteoblastic differentiation in vitro. Pairwise datasets representing changes in gene expression associated with growth arrest (day 2 to 5 in culture), differentiation (day 5 to 10 in culture), and osteoblast maturation (day 10 to 28 in culture) were analyzed using Ingenuity Systems Pathways Analysis to generate predictions about signaling pathway activity based on the temporal sequence of changes in target gene expression. Our data indicate that some pathways involved in osteoblast differentiation, e.g. Wnt/β-catenin signaling, are most active early in the process, while others, e.g. TGFβ/BMP, cytokine/JAK-STAT and TNFα/RANKL signaling, increase in activity as differentiation progresses. Collectively, these pathways contribute to the sequential expression of genes involved in the synthesis and mineralization of extracellular matrix. These results provide insight into the temporal coordination and complex interplay between signaling networks controlling gene expression during osteoblast differentiation. A more complete understanding of these processes may aid the discovery of novel methods to promote osteoblast development for the treatment of conditions characterized by low bone mineral density.
骨重建涉及破骨细胞的协同作用,破骨细胞吸收矿化的骨基质,成骨细胞填充破骨细胞造成的侵蚀坑,以恢复骨骼完整性并适应机械负荷的变化。成骨细胞来源于多能间充质干细胞前体,在许多局部和环境线索的影响下进行分化。为了描述与成骨细胞成熟和功能相关的自分泌/旁分泌信号网络,我们使用互补的“无偏”DNA 微阵列和源自体外诱导同步成骨分化的鼠 MC3T3-E1 细胞的“靶向”NanoString nCounter 数据集进行基因网络分析。使用 Ingenuity Systems Pathways Analysis 分析代表与生长停滞(培养第 2 至 5 天)、分化(培养第 5 至 10 天)和成骨细胞成熟(培养第 10 至 28 天)相关的基因表达变化的成对数据集,根据靶基因表达变化的时间顺序生成关于信号通路活性的预测。我们的数据表明,一些与成骨细胞分化相关的途径,例如 Wnt/β-catenin 信号通路,在该过程早期最为活跃,而其他途径,例如 TGFβ/BMP、细胞因子/JAK-STAT 和 TNFα/RANKL 信号通路,则随着分化的进展而增加活性。这些途径共同促进参与细胞外基质合成和矿化的基因的顺序表达。这些结果提供了对控制成骨细胞分化过程中基因表达的信号网络的时间协调和复杂相互作用的深入了解。对这些过程的更全面理解可能有助于发现促进成骨细胞发育的新方法,以治疗骨密度低的疾病。