Posterior capsular opacification (PCO) is the leading cause of vision loss after cataract, mainly caused by the adhesion, proliferation and trans-differentiation of post-operative residual lens epithelial cells (LECs). Effective PCO prevention remains a huge challenge to ophthalmologists and researches for decades. Herein, we developed a “NIR-triggered ROS storage” intraocular implant (CTR-Py-PpIX) based on capsular tension ring (CTR), which is concurrently linked with photosensitizer protophorphyrin IX (PpIX) and energy storage 2-pyridone derivative (Py), to guarantee instantaneous and sustainable ROS generation for LECs killing, aiming to achieve more efficient and safer photodynamic therapy (PDT) to effectively prevent PCO. The silylated PpIX-Si and Py-Si were covalently conjugated to the plasma activated CTR surface to obtain CTR-Py-PpIX. Results demonstrated that CTR-Py-PpIX had dual functions of PDT and battery, in which PpIX could generate ROS extracellularly under irradiation, with one part directly inhibiting LECs by lipid peroxidation (LPO) induction of cell membranes. Meanwhile, the excess ROS stored in Py could be continuously released to amplify LPO levels after the irradiation was removed. Ultimately, the proliferation of LECs in capsular bag was completely inhibited under mild irradiation conditions, achieving a sustainable and controlled PDT effect for effective PCO prevention with good biocompatibility. This NIR-triggered ROS storage intraocular implant would provide a more efficient and safer approach for long-term PCO prevention.
Peripheral nerves and blood vessels regulate the development process of bone tissue by delivering neural and vascular-related cytokines. However, challenge of preventing the loss of neural and vascular growth factors and ensuring their long-term availability for bone defects was often been overlooked. The current study designed a hybrid cell membrane with specific surface receptors for calcitonin receptor (CTR) and vascular endothelial growth factor receptor (VEGFR) through overexpressed the CTR receptor gene ( Calcr ) and the VEGFR 1 gene ( Flt-1 ). The bone repair matrix functionalized by the hybrid cell membrane (GCMs) had collecting property for neurogenic growth factor (NGF) and vascular endothelial growth factor (VEGF). Furthermore, GCMs enhanced neural and vascular differentiation in mesenchymal stem cells (MSCs) and stimulated osteogenic differentiation of MSCs through neural and vascular-related paracrine signals. GCMs also facilitated the angiogenesis and neurogenesis around bone defects, further promoted the repair of rat skull defects. This study suggests a promising approach for using cell membranes to harvest growth factors for innervation and vascularization in bone reconstruction.
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