Objective: Although emerging evidence suggests that both osteoarthritis (OA) and brain atrophy (as assessed by structural neuroimaging markers) are associated with the risk of dementia, little is known about the association between OA and structural neuroimaging markers. This study aimed to examine the association of OA with changes in structural neuroimaging markers among non-demented older people.Methods: We examined the cross-sectional and longitudinal associations between OA and structural neuroimaging markers (hippocampal volume, entorhinal volume, ventricular volume, and volume of gray matter of the whole brain) among non-demented older people. We categorized our participants as those without OA (OA−) and those with OA (OA+). At baseline, we included 1,281 non-demented older adults, including 1,050 without OA and 231 with OA.Results: In the cross-sectional analysis, we did not observe any significant difference in structural neuroimaging markers between the two OA groups. In the longitudinal analysis, we found that compared to participants without OA, those with OA showed a steeper decline in volumes of the gray matter of the whole brain among non-demented older adults.Conclusions: OA was associated with a steeper decline in volumes of the gray matter of the whole brain over time among non-demented older people.
Objective Osteochondral decellularization can promote local vascular regeneration, but the exact mechanism is unknown. The aim of this study is to study osteogenic microvascular regeneration in single cells. Methods The scRNA-seq dataset of human periosteal-derived cells (hPDCs) were analyzed by pySCENIC. To examine the role of TBX3 in osteogenesis and vascularization, cell transfection, qRT-PCR, western blot, and CCK-8 cell proliferation assays were performed. Results TCF7L2, TBX3, FLI1, NFKB2, and EZH2 were found to be transcription factors (TFs) most closely associated with corresponding cells. The regulatory network of these TFs was then visualized. Our study knocked down the expression of TBX3 in human osteoblast cell lines. In the TBX3 knockdown group, we observed decreased expression of VEGFA, VEGFB, and VEGFC. Moreover, Western blot analysis showed that downregulating TBX3 resulted in a reduction of VEGFA expression. And TBX3 stimulated osteoblast proliferation in CCK-8 assays. Conclusion TBX3 regulates VEGFA expression and promotes osteoblast proliferation in skeletal microvasculature formation. The findings provide a theoretical basis for investigating the role of TBX3 in promoting local vascular regeneration.
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