Lu Jia-Jie, Zhang Qi-Chen, Yuan Guang-Cheng, Zhang Tai-Wei, Huang Yu-Kai, Wu Tao, Su Di-Han, Dong Jian, Jiang Li-Bo, Li Xi-Lei
Department of Orthopaedic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Department of Orthopaedic Surgery, Shanghai Baoshan District Wusong Center Hospital, Fudan University, Shanghai, 200940, China.
Mater Today Bio. 2024 Sep 14;29:101252. doi: 10.1016/j.mtbio.2024.101252. eCollection 2024 Dec.
Nucleus pulposus (NP) cells, situated at the core of intervertebral discs, have acclimated to a hypoxic environment, orchestrating the equilibrium of extracellular matrix metabolism (ECM) under the regulatory influence of hypoxia inducible factor-1α (HIF-1α). Neovascularization and increased oxygen content pose a threat, triggering ECM degradation and intervertebral disc degeneration (IVDD). To address this, our study devised an oxygen-controllable strategy, introducing laccase into an injectable and ultrasound-responsive gelatin/agarose hydrogel. Laccase-mediated reactions were employed to deplete oxygen, establishing a hypoxic microenvironment that upregulated HIF-1α expression. The activation of hypoxia-inducible factors significantly enhanced the expression of aggrecan and collagen II, concurrently suppressing Matrix metalloproteinases (MMP13) and A Disintegrin and Metalloproteinase with Thrombospondin motifs (ADAMTS5) levels, thereby restoring the equilibrium of ECM metabolism. Simultaneously, the hydrogel facilitated the recruitment of stem cells into the NP through the controlled release of ATI2341, activating C-X-C chemokine receptor type 4 (CXCR4). Moreover, ultrasound amplification enhanced ATI2341 release, promoting the migration of NP stem cells. The hydrogel's efficacy in mitigating metabolic imbalances and inhibiting IVDD progression was substantiated in a rat puncture IVDD model through hydrogel injection into the discs. In conclusion, this hypoxia-inducible hydrogel, responsive to thermal stimuli from ultrasound, presents a promising avenue for IVDD treatment.
髓核(NP)细胞位于椎间盘的核心部位,已适应低氧环境,在缺氧诱导因子-1α(HIF-1α)的调节作用下协调细胞外基质代谢(ECM)的平衡。新生血管形成和氧含量增加构成威胁,引发ECM降解和椎间盘退变(IVDD)。为解决这一问题,我们的研究设计了一种氧可控策略,将漆酶引入可注射且对超声有响应的明胶/琼脂糖水凝胶中。利用漆酶介导的反应消耗氧气,建立上调HIF-1α表达的低氧微环境。缺氧诱导因子的激活显著增强了聚集蛋白聚糖和胶原蛋白II的表达,同时抑制基质金属蛋白酶(MMP13)和含血小板反应蛋白基序的解聚素和金属蛋白酶(ADAMTS5)的水平,从而恢复ECM代谢的平衡。同时,水凝胶通过可控释放ATI2341促进干细胞向NP募集,激活C-X-C趋化因子受体4(CXCR4)。此外,超声放大增强了ATI2341的释放,促进了NP干细胞的迁移。通过向大鼠穿刺IVDD模型的椎间盘内注射水凝胶,证实了水凝胶在减轻代谢失衡和抑制IVDD进展方面的功效。总之,这种对超声热刺激有响应的缺氧诱导水凝胶为IVDD治疗提供了一条有前景的途径。