Reprogramming mitochondrial metabolism of macrophages by miRNA-released microporous coatings to prevent peri-implantitis.
Hongming ZhangYun YuanHanxiao XueRunping YuXiayue JinXiaolin WuHui HuangPublished in: Journal of nanobiotechnology (2023)
Although various new biomaterials have enriched the methods for peri-implant inflammation treatment, their efficacy is still debated, and secondary operations on the implant area have also caused pain for patients. Recently, strategies that regulate macrophage polarization to prevent or even treat peri-implantitis have attracted increasing attention. Here, we prepared a laser-drilled and covered with metal organic framework-miR-27a agomir nanomembrane (L-MOF-agomir) implant, which could load and sustain the release of miR-27a agomir. In vitro, the L-MOF-agomir titanium plate promoted the repolarization of LPS-stimulated macrophages from M1 to M2, and the macrophage culture supernatant promoted BMSCs osteogenesis. In a ligation-induced rat peri-implantitis model, the L-MOF-agomir implants featured strong immunomodulatory activity of macrophage polarization and alleviated ligation-induced bone resorption. The mechanism of repolarization function may be that the L-MOF-agomir implants promote the macrophage mitochondrial function and metabolism reprogramming from glycolysis to oxidative phosphorylation. Our study demonstrates the feasibility of targeting cell metabolism to regulate macrophage immunity for peri-implantitis inhibition and provides a new perspective for the development of novel multifunctional implants.
Keyphrases
- metal organic framework
- soft tissue
- oxidative stress
- cell proliferation
- diabetic rats
- long non coding rna
- adipose tissue
- high glucose
- long noncoding rna
- end stage renal disease
- newly diagnosed
- chronic pain
- ejection fraction
- bone regeneration
- mesenchymal stem cells
- pain management
- prognostic factors
- inflammatory response
- bone mineral density
- cell therapy
- cancer therapy
- postmenopausal women
- bone loss
- patient reported outcomes
- spinal cord injury
- stress induced
- protein kinase