Surface topography and chemistry have significant influences on the biological performance of biomedical implants. Our aim is to produce an implant surface with favorable biological properties by dual modification of surface chemistry and topography in one single simple process. In this study, because of its chemical stability, excellent corrosion resistance, and biocompatibility, titanium oxide (TiO2) was chosen to coat the biomedical Ti alloy implants. Biocompatible elements (niobium (Nb) and silicon (Si)) were introduced into TiO2 matrix to change the surface chemical composition and tailor the thermophysical properties, which in turn leads to the generation of topographical features under specific thermal history of plasma spraying. Results demonstrated that introduction of Nb2O5 resulted in the formation of Ti0.95Nb0.95O4 solid solution and led to the generation of nanoplate network structures on the composite coating surface. By contrast, the addition of SiO2 resulted in a hairy nanostructure and coexistence of rutile and quartz phases in the coating. Additionally, the introduction of Nb2O5 enhanced the corrosion resistance of TiO2 coating, whereas SiO2 did not exert much effect on the corrosion behaviors. Compared to the TiO2 coating, TiO2 coating doped with Nb2O5 enhanced primary human osteoblast adhesion and promoted cell proliferation, whereas TiO2 coatings with SiO2 were inferior in their bioactivity, compared to TiO2 coatings. Our results suggest that the incorporation of Nb2O5 can enhance the biological performance of TiO2 coatings by changing the surface chemical composition and nanotopgraphy, suggesting its potential use in modification of biomedical TiO2 coatings in orthopedic applications.
Optimization of the carbon dots synthetic parameters, including type of solvent, heating time, dopant quantity, and particle size distribution range, to gain a better understanding of their effect on carbon dots photophysical and biological behavior.
Abstract Combating the accumulated senescent cells and the healing of osteoporotic bone fractures in the older remains a significant challenge. Nicotinamide mononucleotide (NMN), a precursor of NAD+, is an excellent candidate for mitigating aging-related disorders. However, it is unknown if NMN can alleviate senescent cell induction and enhance osteoporotic bone fracture healing. Here we show that NMN treatment partially reverses the effects of tumor necrosis factor-alpha (TNF-α) on human primary osteoblasts (HOBs): senescent cell induction, diminished osteogenic differentiation ability, and intracellular NAD+ and NADH levels. Mechanistically, NMN restores the mitochondrial dysfunction in HOBs induced by TNF-α evidenced by increased mitochondrial membrane potential and reduced reactive oxidative species and mitochondrial mass. NMN also increases mitophagy activity by down-regulating P62 expression and up-regulating light chain 3B-II protein expression. In addition, the cell senescence protective effects of NMN on HOBs are mitigated by a mitophagy inhibitor (Bafilomycin A1). In vivo, NMN supplementation attenuates senescent cell induction in growth plates, partially prevents osteoporosis in an ovariectomized mouse model, and accelerates bone healing in osteoporotic mice. We conclude that NMN can be a novel and promising therapeutic candidate to enhance bone fracture healing capacity in the older.
In recent years, the development of carbon dot‐based fluorescent nanoparticles for bioimaging applications has attracted the attention of the scientific community. However, many of these systems absorb and emit in the blue–green region of the electromagnetic spectrum, limiting their application in bioimaging. Herein, the facile design and development of highly efficient two‐photon excitable red‐emissive carbon dots are reported and their high performance in bioimaging applications is demonstrated. The importance of aromatic precursors in developing red‐emissive carbon dots is demonstrated. The optimized carbon dots are highly biocompatible and nontoxic, with remarkable photostability in cells under two‐photon near‐infrared excitation. The present study points to the great potential of two‐photon excitable red‐emissive carbon dot as an efficient bioimaging agent for cellular biolabeling, long‐term and real‐time cellular imaging, and high‐resolution deep‐tissue imaging in complex biological systems.
Bone fractures and critical-sized bone defects present significant health threats for the elderly who have limited capacity for regeneration due to the presence of functionally compromised senescent cells. A wide range of synthetic materials has been developed to promote the regeneration of critical-sized bone defects, but it is largely unknown if a synthetic biomaterial (scaffold) can modulate cellular senescence and improve bone regeneration in aged scenarios. The current study investigates the interaction of Baghdadite (Ca3ZrSi2O9) ceramic scaffolds with senescent human primary osteoblast-like cells (HOBs) and its bone regeneration capacity in aged rats. A senescent HOB model was established by repeatedly passaging HOBs till passage 7 (P7). Compared to the clinically used hydroxyapatite/tricalcium phosphate (HA/TCP), Baghdadite prevented senescence induction in P7 HOBs and markedly negated the paracrine effect of P7 HOB secretomes that mediated the up-regulations of cellular senescence-associated gene expression levels in P2 HOBs. We further demonstrated that conditioned media extracted from Baghdadite corrected the dysfunctional mitochondria in P7 HOBs. In vivo, the bone regeneration capacity was enhanced when 3D printed Baghdadite scaffolds were implanted in a calvaria critical-sized bone defect model in both young and aged rats compared to HA/TCP scaffolds, but a better effect was observed in aged rats than in young rats. This study suggests that Baghdadite ceramic represents a novel and promising biomaterial approach to promote bone regeneration capacity in the elderly by providing an anti-senescent microenvironment.
Ideally, biomaterials have inductive properties, favoring specific lineage differentiation. For chondrogenic induction, these properties have been attributed to collagen type II. However, the underlying mechanisms are largely unknown. This study aimed to investigate whether collagen type II favors chondrogenic induction by affecting cell shape through β1 integrins and Rho A/Rock signaling. For this purpose, adipose tissue–derived stem cells (ASCs) were encapsulated in collagen type I or II gels and cultured in plain and chondrogenic medium. It was demonstrated that (i) ASCs showed more efficient chondrogenic induction (higher collagen X, aggrecan, sox6, sox9, and collagen II gene expression) in both plain and chondrogenic media in collagen type II versus collagen type I gels; (ii) ASCs showed lower Rock 2 gene expression and a more rounded cell shape in collagen type II versus type I gels when grown in plain medium; (iii) Rock inhibitor (Y27632) more effectively enhanced chondrogenic gene expression of ASCs in collagen type I than in collagen type II gels, and diminished differences in chondrogenic gene expression and cell shape of ASCs between the two gel types; and (iv) β1 integrins blocking not only reduced the differences of chondrogenic gene expression but also eliminated the differences of Rock 1 and Rock 2 gene expressions and cell shape when comparing ASCs embedded in collagen type I and II gels. We conclude that collagen type II provides the inductive signaling for chondrogenic differentiation in ASCs by evoking a round cell shape through β1 integrin–mediated Rho A/Rock signaling pathway.
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