Traffic accidents, falls, and many other events may cause traumatic spinal cord injuries (SCIs), resulting in nerve cells and extracellular matrix loss in the spinal cord, along with blood loss, inflammation, oxidative stress (OS), and others. The continuous development of neural tissue engineering has attracted increasing attention on the application of fibrin hydrogels in repairing SCIs. Except for excellent biocompatibility, flexibility, and plasticity, fibrin, a component of extracellular matrix (ECM), can be equipped with cells, ECM protein, and various growth factors to promote damage repair. This review will focus on the advantages and disadvantages of fibrin hydrogels from different sources, as well as the various modifications for internal topographical guidance during the polymerization. From the perspective of further improvement of cell function before and after the delivery of stem cell, cytokine, and drug, this review will also evaluate the application of fibrin hydrogels as a carrier to the therapy of nerve repair and regeneration, to mirror the recent development tendency and challenge.

The materials used in bone tissue engineering (BTE) have been advancing with each passing day. With the continuous development of nanomedicine, gold nanoparticles (GNPs), which are easy to be synthesized and functionalized, have attracted increasing attention. Recent years have witnessed this amazing material, i.e., GNPs characterized with large surface area to volume ratio, biocompatibility, medical imaging property, hypotoxicity, translocation into the cells, high reactivity, and other properties, perform distinct functions in BTE. However, the low stability of GNPs in the biotic environment makes them in the requirements of modification or recombination before being used. After being combined with the advantages of other materials, the structures of GNPs have exhibited great potential in stem cells, scaffolds, delivery systems, medical imaging, and other aspects. This review will focus on the advances in the application of GNPs after modification or recombination with other materials to BTE.

At present, the healing of osteopathy, especially the healing of cartilage, has been proven to be difficult. Commonly used treatment methods are autogenous bone grafts and allogeneic bone grafts, but grafts cannot fully meet the clinical treatment requirements due to problems related to the source, price, immunity, and other concerns. Thus, the combination of biomaterials and tissue engineering technology has become a new direction in research. Among studies on tissue engineering bone and cartilage materials, hydrogels that show biological activity, absorbability after degradability, plasticity, and easy preparation have become the focus. Hydrogels are used as extracellular matrix mimics. Although various materials are able to form hydrogels, hyaluronic acid and its derivatives are prominently used. Hyaluronic acid hydrogels have many advantages, such as promoting cell adhesion and proliferation and wound healing. They also demonstrate sufficient biological activity for stimulating a microenvironment for cell survival. However, their disadvantages require further modification and include a poor degradation rate and insufficient mechanical performance. In this paper, hyaluronic acid-based hydrogels, their modifications, applications, and mechanisms, as well as new techniques for processing hyaluronic acid hydrogels in bone and cartilage tissue engineering, are briefly reviewed, and their future prospects and directions for future work are discussed.

Background: Excessive light exposure is a detrimental environmental factor that plays a critical role in the pathogenesis of retinal degeneration. However, the mechanism of light-induced death of retina/photoreceptor cells remains unclear. The mammalian/mechanistic target of rapamycin (mTOR) and Poly (ADP-ribose) polymerase-1 (PARP-1) have become the primary targets for treating many neurodegenerative disorders. The aim of this study was to elucidate the mechanisms underlying light-induced photoreceptor cell death and whether the neuroprotective effects of mTOR and PARP-1 inhibition against death are mediated through apoptosis-inducing factor (AIF). Methods: Propidium iodide (PI)/Hoechst staining, lentiviral-mediated short hairpin RNA (shRNA), Western blot analysis, cellular fraction separation, plasmid transient transfection, laser confocal microscopy, a mice model, electroretinography (ERG), and hematoxylin-eosin (H & E) staining were employed to explore the mechanisms by which rapamycin/3-Aminobenzamide (3AB) exert neuroprotective effects of mTOR/PARP-1 inhibition in light-injured retinas. Results: A parthanatos-like death mechanism was evaluated in light-injured 661 W cells that are an immortalized photoreceptor-like cell line that exhibit cellular and biochemical feature characteristics of cone photoreceptor cells. The death process featured over-activation of PARP-1 and AIF nuclear translocation. Either PARP-1 or AIF knockdown played a significantly protective role for light-damaged photoreceptors. More importantly, crosstalk was observed between mTOR and PARP-1 signaling and mTOR could have regulated parthanatos via the intermediate factor sirtuin 1 (SIRT1). The parthanatos-like injury was also verified in vivo, wherein either PARP-1 or mTOR inhibition provided significant neuroprotection against light-induced injury, which is evinced by both structural and functional retinal analysis. Overall, these results elucidate the mTOR-regulated parthanatos death mechanism in light-injured photoreceptors/retinas and may facilitate the development of novel neuroprotective therapies for retinal degeneration diseases. Conclusions: Our results demonstrate that inhibition of the mTOR/PARP-1 axis exerts protective effects on photoreceptors against visible-light–induced parthanatos. These protective effects are conducted by regulating the downstream factors of AIF, while mTOR possibly interacts with PARP-1 via SIRT1 to regulate parthanatos. Graphical Schematic diagram of mTOR interacting with PARP-1 to regulate visible light-induced parthanatos. Increased ROS caused by light exposure penetrates the nuclear membrane and causes nuclear DNA strand breaks. PARP-1 detects DNA breaks and synthesizes PAR polymers to initiate the DNA repair system that consumes a large amount of cellular NAD+. Over-production of PAR polymers prompts the release of AIF from the mitochondria and translocation to the nucleus, which leads to parthanatos. Activated mTOR may interact with PARP-1 via SIRT1 to regulate visible light-induced parthanatos.

Electrical stimulation (ES) and insulin-like growth factor-1 (IGF-1) are widely used in bone regeneration because of their osteogenic activity. However, the combined effects of ES and supplemental IGF-1 on the whole bone formation process remain unclear. In this study, fluorescence staining and an MTT assay were first utilized to observe the influence of ES and IGF-1 on MC3T3-E1 cell proliferation and adhesion in vitro. Subsequently, osteogenic differentiation was evaluated by the alkaline phosphatase activity (ALP) and the expression of osteogenic marker genes. In addition, cell mineralization was determined by alizarin red staining and scanning electron microscopy (SEM). We demonstrated that the MC3T3-E1 cell proliferation was significantly higher for treatments combining IGF-1 and ES than for treatments with IGF-1 alone. The combination of IGF-1 and ES increased the MC3T3-E1 cell ALP activity, the expression of osteogenesis-related genes and the calcium deposition with a clear dose-dependent effect. Our data show the synergistic effect of IGF-1 and ES in promoting the proliferation, differentiation and mineralization of MC3T3-E1 cells, which suggests that it would be more effective to combine the proper dose of IGF-1 with ES to promote local bone damage repair and regeneration.

Chitosan (CS) is a natural polymer with applications in wound restorations and coatings for artificial implants. However, the lack of antimicrobial activity restricts its further application. Thus, the purpose of this study is to prepare CS/AuNPs film by adding gold nanoparticles (AuNPs) to modify chitosan. Through transmission electron microscopy, we found that the presence of CS can effectively prevent the agglomeration of nanoparticles. Furthermore, through the CCK experiment, we found that AuNPs at a certain concentration can improve the adhesion and proliferation of cells, which has also been proved in animal experiments, including gross appearance, histological observations, and immunofluorescence staining. Such findings support the feasibility of using the film as a promising candidate for tissue engineering of skin in a near future.