Effect of micropore/microsphere topography and a silicon-incorporating modified titanium plate surface on the adhesion and osteogenic differentiation of BMSCs

AbstractGood biological properties for titanium implants will shorten the treatment cycle and improve patient comfort, which are also the main goals of dentistry and orthopaedics. At present, the biological properties of titanium implants are mainly enhanced in two aspects: their surface chemistry and surface morphology. In this study, a surface modification strategy combining bioactive trace elements with surface micromorphology modification was used to enhance the biological properties of pure titanium. A new coating incorporating silicon micropore/microsphere topography was prepared on a titanium plate by micro-arc oxidation (MAO) technology. The properties of the coating and its effects on the adhesion and osteogenic differentiation of rat bone marrow mesenchymal stem cells (BMSCs) were further analyzed. The experimental results show that a coating doped with amorphous silicon with micropore/microsphere topography was incorporated onto the titanium surface and the surface roughness in the treated groups was obviously higher than that in the Ti group. In vitro, the presence of a silicon-incorporating coating with a micropore/microsphere topography on the titanium surface significantly enhanced the initial adhesion, proliferation and osteogenic differentiation of BMSCs. These results indicate that the silicon-incorporating coating with micropore/microsphere topography has potential applications in dentistry and orthopaedics

CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice

Abstract CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. However, our bone marrow transplantation assay showed that CD38 deficiency in lymphocytes led to lack of protection against Ang II-induced vascular remodeling, suggesting that the effects of CD38 on Ang II-induced vascular remodeling might rely primarily on vascular smooth muscle cells (VSMCs), not lymphocytes. In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs. Furthermore, we found that the protective effects of CD38 deficiency on VSMC senescence were related to restoration of lysosome dysfunction, particularly with respect to the maintenance of sirtuin-mediated mitochondrial homeostasis and activation of the mitochondria–lysosomal axis in VSMCs. In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling