抗氧化酶 Prdx1 通过抑制 ROS 和 NFATc1 信号通路抑制破骨细胞生成

IF 4.5 2区生物学 Q2 CELL BIOLOGY

Journal of Cellular Physiology Pub Date : 2024-09-12 DOI:10.1002/jcp.31431

Chao Wang, Gang Wang, Fangming Song, Jinmin Zhao, Qian Liu, Jiake Xu

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引用次数: 0

摘要

骨骼是一个动态器官，在人的一生中会不断发生重塑。细胞产生的活性氧（ROS）对调节骨平衡至关重要。破骨细胞是由巨噬细胞分化而来的多核巨细胞，是溶骨性骨病的罪魁祸首，而溶骨性骨病与 ROS 信号通路密切相关。本研究发现，骨髓巨噬细胞和破骨细胞中都表达一种抗 ROS 的酶--过氧化还原酶 1（Prdx1）。研究发现，重组 Prdx1 蛋白可剂量依赖性地抑制 ROS 的产生和破骨细胞的分化。从机制上讲，Prdx1 蛋白还能抑制 NFATc1 的激活以及 C-Fos、V-ATPase-d2、Cathepsin K 和 Integrin αV 的表达。总之，Prdx1 通过抑制 RANKL 介导的 ROS 活性对破骨细胞的形成具有负向调节作用，因此它有可能应用于治疗破骨细胞相关疾病。

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Antioxidant enzyme Prdx1 inhibits osteoclastogenesis via suppressing ROS and NFATc1 signaling pathways

Bone is a dynamic organ which continuously undergoes remodeling throughout one's lifetime. Cellular production of reactive oxygen species (ROS) is essential for regulating bone homeostasis. Osteoclasts, multinucleated giant cells differentiated from macrophage lineage, are responsible for osteolytic bone conditions which are closely linked to ROS signaling pathways. In this study, an anti‐ROS enzyme, peroxiredoxin 1 (Prdx1) was found to be expressed both in bone marrow macrophages and osteoclasts. Recombinant Prdx1 protein was found to dose‐dependently inhibit ROS production and osteoclast differentiation. Mechanistically, Prdx1 protein also attenuated NFATc1 activation as well as the expression of C‐Fos, V‐ATPase‐d2, Cathepsin K, and Integrin αV. Collectively, Prdx1 is a negative regulator on osteoclast formation via inhibiting RANKL‐mediated ROS activity, thus suggesting its potential application for treating osteoclast related disorders.

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来源期刊

Journal of Cellular Physiology 生物-生理学

CiteScore

14.70

自引率

0.00%

发文量

256

审稿时长

1 months

期刊介绍： The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.