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Our study intends to explore the effect of bone marrow mesenchymal stem cells (BMSCs) on neuronal activity and GDNF expression in rats with SCI. Rats were assigned into spinal cord injury group (group S); routinely control group (group R) without spinal incision; and BMSCs group (group B) which received BMSCs treatment with n = 4 rats in each group. The neuronal cell proliferation was detected by cck-8 method, BBB score was used to detect lower limb motor function, GDNF mRNA expression was detected by qRT-PCR, GDNF protein positive expression was measured by immunohistochemistry and cell invasion was assessed by Transwell. Group B rats showed significantly higher BBB score higher than group S (P P P P P P P P P P

Bone remodeling participates in osteoporosis (OP). Silent information regulating factor 2 related enzyme 1 (sirtuin1, SIRT1) regulates cell survival, differentiation, metabolism and inflammation. However, the regulatory effect of SIRT1 on the formation of osteoblasts and osteoclasts has not been reported. OP and normal rat BMSCs were assigned into control group, OP group, and SIRT1 group (Resveratrol) followed by measuring cell proliferation by MTT assay, ALP activity, expression of SIRT1, RUNX2 and OP by Real time PCR, AKT/β-catenin signaling protein expression by Western blot. Rat BMSCs were cultured and treated with RANKL to induce osteoclast culture in the presence or absence of Resveratrol followed by analysis of cell proliferation and c-Fos and TRAP expression. SIRT1 expression and secretion in BMSCs cells and supernatant of OP group were significantly reduced and cell proliferation was significantly inhibited along with reduced RUNX2 and OP expression, ALP activity as well as decreased AKT/β-catenin phosphorylation compared to control group (P < 0.05); addition of Resveratrol can significantly reverse the above changes (P P < 0.05). SIRT1 expression is reduced in osteoporosis and its upregulation promotes osteogenesis through AKT/β-catenin pathway, inhibits osteoclast formation, and improves osteoporosis.

Background Calcium polyphosphate (CPP) is a commonly used biomaterial in bone tissue engineering, but CPP is insufficient in osteoinduction. This study aimed to fabricate lithium doped CPP (LiCPP) scaffolds and assess their characterization, degradation, biocompatibility and osteogenesis behavior for bone tissue engineering. Methods The novel scaffold was characterized by XRD, FTIR and SEM. The porosity, cell mediated degradation behavior and mechanical properties were also investigated. Meanwhile, cell proliferation activity and adhesion in vitro was exploited. Finally, osteogenesis the LiCPP scaffolds in vitro and in vivo was researched. Results The outcomes revealed that low-content Li doping had no significant influence on the structure of CPP. The results of cells mediated degradation experiments from the weight loss and the release of ions indicated that Li doped CPP improved biological degradation. The compressive strength of CPP with 66% porosity was improved to 7 MPa. Cells proliferation experiment and adhesion experiment demonstrated 2.0%LiCPP scaffold was most beneficial to cell growth and attachment. Furthermore, Li doped CPP up-regulated Wnt signal pathway when co-cultured with MG63 and increased osteogenic marker ALP expression and calcium phosphate deposition in vitro. At the same time, new bone formation in vivo was also enhanced by using LiCPP scaffolds and the 2.0%LiCPP scaffolds obtained best osteogenesis outcomes. Conclusion The results obtained in our study suggest that 2.0%LiCPP scaffold could benefit from improving the osteogenesis behavior and is a promising biomaterial for bone repairing applications.

Intervertebral disc degeneration (IVDD) is a main cause of low back pain that is associated with extracellular matrix (ECM) degradation and inflammation. This study aims to investigate the role of DNMT3B and its regulatory mechanisms in IVDD. IVDD rat models were constructed followed by transfections with oe-DNMT3B or oe-YAP in order to explore the role of DNMT3B in the development of IVDD. After that transfection, nucleus pulposus (NP) cells were isolated and transfected with oe-DNMT3B, oe-TRPA1, si-YAP, oe-YAP or oe-COX2 in order to investigate the functions of DNMT3B in NP cells. DNMT3B was poorly expressed in IVDD tissues and NP cells whereas TRPA1, COX2, and YAP were highly expressed. The proliferation or apoptosis of NP cells was detected through CCK-8 assay or flow cytometry, respectively. Overexpression of DNMT3B promoted the proliferation of NP cells, inhibited their apoptosis, as well as increasing the expression of collagen II and aggrecan and decreasing expression of MMP3 and MMP9. Besides, DNMT3B suppressed inflammation and alleviated IVDD. Mechanistically, DNMT3B modified the TRPA1 promoter by methylation to inhibit the expression of COX2. Overexpression of COX2 promoted the apoptosis of NP cells and decreased the expression of YAP, which was reversed by upregulating DNMT3B. DNMT3B may promote the proliferation of NP cells and prevent their ECM degradation through the TRPA1/COX2/YAP axis, thereby alleviating IVDD in rats.