Zheng Jiancheng, Li Xiaoyan, Zhang Fangke, Li Changwei, Zhang Xingkai, Wang Fei, Qi Jin, Cui Wenguo, Deng Lianfu
Department of Orthopaedics Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics Ruijin Hospital, 197 Ruijin 2nd Road, Shanghai, 200025, P. R. China.
Department of Orthopedic, Affiliated Hospital of Jining Medical University, Jining City, Shandong Province, 272029, P. R. China.
Adv Healthc Mater. 2024 Dec;13(31):e2402117. doi: 10.1002/adhm.202402117. Epub 2024 Aug 18.
Balancing osteoblast-osteoclast (OB-OC) cross-talk is crucial for restoring bone tissue structure and function. Current clinical drugs targeting either osteogenesis or osteoclastogenesis fail to effectively regulate cross-talk, impeding efficient bone repair in osteoporosis patients. Ubiquitin-specific protease 26 (USP26) is shown to coordinate OB-OC cross-talk by independently regulating β-catenin and Iκb-α. However, effective drugs for activating USP26 are still lacking. Here, they constructed bone homeostasis repair microcarriers (BHRC) that encapsulate Usp26 mRNA-loaded lipid nanoparticles (mRNA@LNP) within MMPs-responsive GelMA hydrogel microspheres. These microcarriers target the osteoporotic microenvironment and regulate OB-OC cross-talk, thereby facilitating intervertebral fusion in osteoporotic rats. Results demonstrate that mRNA@LNP exhibits uniform particle size and high transfection efficiency, while GelMA hydrogel microspheres possess excellent biocompatibility and MMP responsiveness, providing favorable cell survival space and controllable release of mRNA@LNP. The released LNP upregulates USP26 protein expression, effectively promoting osteogenesis while suppressing osteoclast formation. In vivo experiments show that injecting BHRC into the defect site of intervertebral discs in osteoporotic rats significantly promotes tail vertebrae fusion by responding to the microenvironment and regulating cell-to-cell cross-talk. Thus, the BHRC holds great potential in regulating osteoporotic homeostasis, particularly in challenging bone defects such as intervertebral fusion in osteoporotic environments.
平衡成骨细胞-破骨细胞(OB-OC)之间的相互作用对于恢复骨组织结构和功能至关重要。目前针对骨生成或破骨细胞生成的临床药物无法有效调节这种相互作用,阻碍了骨质疏松患者的有效骨修复。泛素特异性蛋白酶26(USP26)被证明可通过独立调节β-连环蛋白和Iκb-α来协调OB-OC之间的相互作用。然而,仍缺乏激活USP26的有效药物。在此,他们构建了骨稳态修复微载体(BHRC),其在基质金属蛋白酶(MMP)响应性甲基丙烯酸明胶(GelMA)水凝胶微球中包裹了负载Usp26 mRNA的脂质纳米颗粒(mRNA@LNP)。这些微载体靶向骨质疏松微环境并调节OB-OC之间的相互作用,从而促进骨质疏松大鼠的椎间融合。结果表明,mRNA@LNP呈现均匀的粒径和高转染效率,而GelMA水凝胶微球具有优异的生物相容性和MMP响应性,为细胞提供了良好的生存空间并实现了mRNA@LNP的可控释放。释放的LNP上调USP26蛋白表达,有效促进骨生成同时抑制破骨细胞形成。体内实验表明,将BHRC注射到骨质疏松大鼠椎间盘的缺损部位可通过响应微环境和调节细胞间相互作用显著促进尾椎融合。因此,BHRC在调节骨质疏松稳态方面具有巨大潜力,特别是在诸如骨质疏松环境中的椎间融合等具有挑战性的骨缺损方面。