IF 3.5 3区 医学 Q3 CELL & TISSUE ENGINEERING
Jingjing Shao, Shibo Liu, Chenfeng Chen, Wenchuan Chen, Zhimin Zhu, Lei Li
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引用次数: 0

摘要

增强骨-血管耦合以形成高质量的血管丰富的种植体周围骨对于改善老年患者的种植预后至关重要。众所周知,低氧诱导因子1α(HIF1α)可促进骨生成-血管生成耦合;然而,由于HIF1α在不同老年器官中的双重作用,这种作用在老年骨中仍有待研究。本研究以衰老小鼠及其骨间充质干细胞(BMSCs)为研究对象,应用HIF1α抑制剂或激活剂研究衰老状态下HIF1α对植骨周围成骨和血管生成的影响及其内在机制。结果发现,细胞衰老的同时,衰老的BMSCs也具有成骨和血管生成能力。同时,对衰老小鼠构建了股骨植入模型,观察了植入体周围骨的骨-血管耦合。还检测了下颌骨的形态,为临床口腔种植提供了进一步的证据。此外,还对 HIF1α 干预后体内和体外的 p53 表达进行了检测。还采用了一种活性氧(ROS)清除剂来进一步研究 ROS 在 HIF1α-p53 轴中的作用。结果表明,抑制HIF1α可缓解衰老BMSCs的衰老和成骨-血管生成耦合,而激活HIF1α则会加重这些影响。在调节 HIF1α 后,老化种植体周围骨的下颌骨表型和骨-血管耦合也发生了相应的变化。从机理上讲,p53 与 HIF1α 在体内和体外的变化方向相同。此外,ROS 清除剂逆转了 HIF1α 与 p53 的关系,削弱了 HIF1α 抑制剂对种植体周围骨质改善的作用。总之,在老年小鼠中,高表达的 HIF1α 通过 p53 损害了种植体周围骨-血管耦合和种植体骨结合,而积累的 ROS 是 HIF1α 正向调节 p53 的先决条件。这些发现为了解 HIF1α 和 ROS-HIF1α/p53 信号轴的作用提供了新的视角,为改善老年患者的种植效果提供了潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aging Impairs Implant Osseointegration Through a Novel Reactive Oxygen Species-Hypoxia-Inducible Factor 1α/p53 Axis.

Enhancing bone-vessel coupling to form high-quality vascular-rich peri-implant bone is crucial for improving implant prognosis in elder patients. Notably, hypoxia-inducible factor 1α (HIF1α) is known to promote osteogenesis-angiogenesis coupling; however, this effect remains to be investigated in aged bone owing to the dual effect of HIF1α in different aged organs. In this study, HIF1α inhibitor or activator was applied to aged mice and their bone mesenchymal stem cells (BMSCs) to investigate the effects and inner mechanism of HIF1α on the peri-implant osteogenesis and angiogenesis in senescent status. Cell senescence, along with osteogenic and angiogenic abilities of aged BMSCs, was detected, respectively. Meanwhile, a femur implant implantation model was constructed on aged mice, and the bone-vessel coupling of peri-implant bone was observed. Mandibular bone morphology was also detected to further provide evidence for clinical oral implantation. Furthermore, p53 expression was examined in vivo and in vitro following HIF1α intervention. A reactive oxygen species (ROS) scavenger was also adopted to further investigate the roles of ROS in the HIF1α-p53 axis. Results showed that the suppression of HIF1α alleviated senescence and osteogenesis-angiogenesis coupling of aged BMSCs, while its activation aggravated these effects. The mandible phenotype and bone-vessel coupling in aged peri-implant bone also changed accordingly upon regulation of HIF1α. Mechanistically, p53 changed in the same direction as HIF1α in vivo and in vitro. Moreover, the ROS scavenger reversed the HIF1α-p53 relationship and weakened the effect of HIF1α inhibitor on peri-implant bone improvement. In conclusion, in aged mice, highly expressed HIF1α impaired peri-implant bone-vessel coupling and implant osseointegration through p53, and accumulated ROS was a prerequisite for HIF1α to positively regulate p53. These findings provide new insights into the role of HIF1α and the ROS-HIF1α/p53 signaling axis, offering potential therapeutic targets to improve implant outcomes in elderly patients.

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来源期刊
Tissue Engineering Part A
Tissue Engineering Part A Chemical Engineering-Bioengineering
CiteScore
9.20
自引率
2.40%
发文量
163
审稿时长
3 months
期刊介绍: Tissue Engineering is the preeminent, biomedical journal advancing the field with cutting-edge research and applications that repair or regenerate portions or whole tissues. This multidisciplinary journal brings together the principles of engineering and life sciences in the creation of artificial tissues and regenerative medicine. Tissue Engineering is divided into three parts, providing a central forum for groundbreaking scientific research and developments of clinical applications from leading experts in the field that will enable the functional replacement of tissues.
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