Sheng Matilda H-C, Rundle Charles H, Baylink David J, Lau Kin-Hing William
Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, VA Loma Linda Healthcare System, 11201 Benton Street, Loma Linda, CA, 92357, USA.
Department of Medicine and Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA.
Calcif Tissue Int. 2025 Jan 9;116(1):28. doi: 10.1007/s00223-024-01337-7.
This study assessed the novel concept that osteoclast-derived Grem1 has regulatory functions in the skeletal response to calcium stress using an osteoclastic Grem1 conditional knockout (cKO) mouse model. The calcium stress was initiated by feeding cKO mutants and wildtype (WT) littermates a calcium-deficient diet for 2 weeks. Deletion of Grem1 in mature osteoclasts did not affect developmental bone growth nor basal bone turnover. In response to calcium depletion, male cKO mutants showed greater increases in osteoclastic resorption and trabecular bone loss than male WT littermates, indicating an enhanced skeletal sensitivity to calcium depletion in male mutants. The enhanced sensitivity to calcium depletion was sex-dependent, as female cKO mutants showed lower increases in osteoclastic resorption and bone loss than female WT littermates as well as male cKO mutants. The sex disparity in osteoclastic resorption response to calcium stress was intrinsic to osteoclasts since osteoclasts of male but not female cKO mutants showed greater in vitro bone resorption activity than osteoclasts of WT littermates of respective sex. Male cKO mutants displayed smaller bone formation response to calcium depletion than male WT littermates, while female mutants showed bigger bone formation response than female WT littermates, indicating that cKO mutants also displayed sex disparity in bone formation response. The sex disparity in bone formation response was not caused by intrinsic differences in osteoblasts but might be due to sex-dependent differential osteoclastic release of osteogenic factors. In summary, osteoclast-derived gremlin-1 has complicated and sex-dependent regulatory roles in skeletal response to calcium stress.
本研究使用破骨细胞特异性Grem1条件性敲除(cKO)小鼠模型,评估了破骨细胞衍生的Grem1在骨骼对钙应激反应中具有调节功能这一新概念。通过给cKO突变体和野生型(WT)同窝小鼠喂食缺钙饮食2周来引发钙应激。成熟破骨细胞中Grem1的缺失不影响骨骼发育生长,也不影响基础骨转换。在钙缺乏的情况下,雄性cKO突变体比雄性WT同窝小鼠表现出更大的破骨细胞吸收增加和小梁骨丢失,表明雄性突变体骨骼对钙缺乏的敏感性增强。对钙缺乏的敏感性增强具有性别依赖性,因为雌性cKO突变体比雌性WT同窝小鼠以及雄性cKO突变体表现出更低的破骨细胞吸收增加和骨丢失。破骨细胞对钙应激的吸收反应中的性别差异是破骨细胞固有的,因为雄性而非雌性cKO突变体的破骨细胞在体外比相应性别的WT同窝小鼠的破骨细胞表现出更大的骨吸收活性。雄性cKO突变体对钙缺乏的骨形成反应比雄性WT同窝小鼠小,而雌性突变体比雌性WT同窝小鼠表现出更大的骨形成反应,表明cKO突变体在骨形成反应中也表现出性别差异。骨形成反应中的性别差异不是由成骨细胞的内在差异引起的,可能是由于破骨细胞释放成骨因子的性别依赖性差异。总之,破骨细胞衍生的gremlin-1在骨骼对钙应激的反应中具有复杂且性别依赖的调节作用。