Department of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan.
WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Nat Commun. 2021 Apr 9;12(1):2136. doi: 10.1038/s41467-021-22402-x.
Osteoclastic bone resorption and osteoblastic bone formation/replenishment are closely coupled in bone metabolism. Anabolic parathyroid hormone (PTH), which is commonly used for treating osteoporosis, shifts the balance from osteoclastic to osteoblastic, although it is unclear how these cells are coordinately regulated by PTH. Here, we identify a serine protease inhibitor, secretory leukocyte protease inhibitor (SLPI), as a critical mediator that is involved in the PTH-mediated shift to the osteoblastic phase. Slpi is highly upregulated in osteoblasts by PTH, while genetic ablation of Slpi severely impairs PTH-induced bone formation. Slpi induction in osteoblasts enhances its differentiation, and increases osteoblast-osteoclast contact, thereby suppressing osteoclastic function. Intravital bone imaging reveals that the PTH-mediated association between osteoblasts and osteoclasts is disrupted in the absence of SLPI. Collectively, these results demonstrate that SLPI regulates the communication between osteoblasts and osteoclasts to promote PTH-induced bone anabolism.
破骨细胞的骨吸收和成骨细胞的骨形成/补充在骨代谢中紧密偶联。甲状旁腺激素(PTH)是一种常用于治疗骨质疏松症的药物,它将平衡从破骨细胞转移到成骨细胞,尽管目前尚不清楚 PTH 如何协调调节这些细胞。在这里,我们确定一种丝氨酸蛋白酶抑制剂,分泌白细胞蛋白酶抑制剂(SLPI),作为一种关键的介质,参与 PTH 介导的向成骨细胞阶段的转变。PTH 可使成骨细胞中 SLPI 高度上调,而 Slpi 的基因缺失严重损害了 PTH 诱导的骨形成。成骨细胞中 SLPI 的诱导增强了其分化,并增加了成骨细胞-破骨细胞的接触,从而抑制了破骨细胞的功能。活体骨成像显示,在缺乏 SLPI 的情况下,PTH 介导的成骨细胞和破骨细胞之间的关联被破坏。总的来说,这些结果表明 SLPI 调节成骨细胞和破骨细胞之间的通讯,以促进 PTH 诱导的骨合成代谢。
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