The positive regulation of bone-forming osteoblast activity and the negative feedback regulation of osteoclastic activity are equally important in strategies to achieve successful alveolar bone regeneration. Here, a molybdenum (Mo)-containing bioactive glass ceramic scaffold with solid-strut-packed structures (Mo-scaffold) was printed, and its ability to regulate pro-osteogenic and anti-osteoclastogenic cellular responses was evaluated in vitro and in vivo. We found that extracts derived from Mo-scaffold (Mo-extracts) strongly stimulated osteogenic differentiation of bone marrow mesenchymal stem cells and inhibited differentiation of osteoclast progenitors. The identified comodulatory effect was further demonstrated to arise from Mo ions in the Mo-extract, wherein Mo ions suppressed osteoclastic differentiation by scavenging reactive oxygen species (ROS) and inhibiting mitochondrial biogenesis in osteoclasts. Consistent with the in vitro findings, the Mo-scaffold was found to significantly promote osteoblast-mediated bone formation and inhibit osteoclast-mediated bone resorption throughout the bone healing process, leading to enhanced bone regeneration. In combination with our previous finding that Mo ions participate in material-mediated immunomodulation, this study offers the new insight that Mo ions facilitate bone repair by comodulating the balance between bone formation and resorption. Our findings suggest that Mo ions are multifunctional cellular modulators that can potentially be used in biomaterial design and bone tissue engineering.
Bone Regeneration ; Cell Differentiation ; Ions/pharmacology* ; Molybdenum/pharmacology* ; Osteoclasts ; Osteogenesis ; Printing, Three-Dimensional ; Tissue Scaffolds/chemistry*

OBJECTIVEThe aim of the study is to improve the anticorrosive property of the dental FeCrMo soft magnetic alloy covered with TiN film obtained by ion beam assisted deposition (IBAD) technology in oral environment.

METHODSThe magnetic force of the FECrMo soft magnetic alloy after TiN film treated were measured by Instron test machine. An advanced electro-chemical method was used to measure the electric potential of corrosion (Ecorr), passive potential (Ep), passive current density (Ip), current density of corrosion (Icorr), polarization resistance (Rp), of FeCrMo soft magnetic alloy in simulated oral environment before and after surface modification.

RESULTSThere were no statistic changes of the magnetic force in 4 groups after alloy with TiN film treated. Comparing with the alloy without surface modified, the Ecorr, Rp of FeCrMo soft magnetic alloy was obviously higher, and the Icorr, Ip and Ep were obviously lower.

CONCLUSIONSThe anticorrosive property of the dental FeCrMo soft magnetic alloy with TiN film is better than that without modified.

Chromium Alloys ; Corrosion ; Dental Alloys ; Dental Prosthesis Retention ; Humans ; Magnetics ; Molybdenum ; Titanium ; pharmacology

BACKGROUND: Melanin is detectable in various sense organs including the skin in animals. It has been reported that melanin adsorbs toxic elements such as mercury, cadmium, and lead. In this study, we investigated the adsorption of molybdenum, which is widely recognized as a toxic element, by melanin. METHODS: Molybdenum level of the mouse skin was measured by inductively coupled plasma mass spectrometry. The pigmentation level of murine skin was digitalized as the L* value by using a reflectance spectrophotometer. An in vitro adsorption assay was performed to confirm the interaction between molybdenum and melanin. RESULTS: Our analysis of hairless mice with different levels of skin pigmentation showed that the level of molybdenum increased with an increase in the level of skin pigmentation (L* value). Moreover, our analysis by Spearman's correlation coefficient test showed a strong correlation (r = - 0.9441, p < 0.0001) between L* value and molybdenum level. Our cell-free experiment using the Langmuir isotherm provided evidence for the adsorption of molybdenum by melanin. The maximum adsorption capacity of 1 mg of synthetic melanin for molybdenum was 131 μg in theory. CONCLUSION Our in vivo and in vitro results showed a new aspect of melanin as an adsorbent of molybdenum.
Adsorption ; Animals ; Melanins ; chemistry ; metabolism ; Mice ; Mice, Hairless ; Mice, Transgenic ; Molybdenum ; chemistry ; metabolism ; pharmacology ; Skin ; chemistry ; drug effects ; Skin Pigmentation ; drug effects ; Water Pollutants, Chemical ; chemistry ; metabolism ; pharmacology

Animals ; Bone and Bones ; drug effects ; Copper ; pharmacology ; therapeutic use ; Fluoride Poisoning ; prevention & control ; Fluorides ; blood ; toxicity ; urine ; Lipid Metabolism ; drug effects ; Molybdenum ; toxicity ; Rabbits ; Trace Elements ; pharmacology ; therapeutic use

Protein-tyrosine phosphatases (PTPs) constitute a family of receptor-like, and cytoplasmic enzymes, which catalyze the dephosphorylation of phosphotyrosine residues in a variety of receptors and signaling molecules. Together with protein tyrosine kinases (PTKs), PTPs are critically involved in regulating many cellular signaling processes. In this study, diverse compounds were screened for PTP inhibition and selectively screened for inhibitors with the end product inhibition properties. Among phosphate analogues and their derivatives for PTP inhibition, Keggin compounds phosphomolybdate (PM) and phosphotungstate (PT) strongly inhibited both PTP-1B and SHP-1, with K(i) values of 0.06-1.2 micromM in the presence of EDTA. Unlike the vanadium compounds, inhibition potencies of PM and PT were not significantly affected by EDTA. PM and PT were potent, competitive inhibitors for PTPs, but relatively poor inhibitors of Ser/Thr phosphatase. Interestingly, PM and PT did not inhibit alkaline phosphatase at all. The crystal structure of PTP-1B in complex with PM, at 2.0 A resolution, reveals that MoO(3), derived from PM by hydrolysis, binds at the active site. The molybdenium atom of the inhibitor is coordinated with six ligands: three oxo-ligands, two apical water molecules and a S atom of the catalytic cysteine residue. In support of the crystallographic finding, we observed that molybdenium oxides (MoO(3), MoO(2), and MoO(2)Cl(2)) inhibited PTP-1B with IC(50) in the range 5-15 micromM.
Binding, Competitive ; Catalytic Domain ; Crystallography, X-Ray ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Edetic Acid/pharmacology ; Enzyme Inhibitors/*pharmacology ; Human ; Inhibitory Concentration 50 ; Kinetics ; Models, Molecular ; Molybdenum/*pharmacology ; Phosphoric Acids/*pharmacology ; Protein Structure, Tertiary ; Protein-Tyrosine-Phosphatase/*antagonists & inhibitors/*chemistry/isolation & purification ; Substrate Specificity ; Tungsten Compounds/*pharmacology