RESULTS: CB-MSCs under both normoglycaemic and hyperglycaemic conditions demonstrated similar morphologies and rapid exponential growth to >300PDs, although high glucose conditions promoted more rapid and persistent proliferation beyond ~50PDs, with few indications of senescence. Limited senescence was confirmed by minimal SA-β-galactosidase staining, low senescence marker (p53, p21waf1, p16INK4a) expression and positive telomere maintenance marker (rTERT, TR) expression. However, telomere lengths varied throughout culture expansion, with hyperglycaemia significantly reducing telomere lengths at PD50 and PD200. Furthermore, CB-MSCs expanded in normal and high glucose conditions remained non-transformed, exhibiting similar MSC (CD73/CD90/CD105), multipotency (CD146) and embryonic (Slug, Snail) markers throughout extended culture, but negligible hematopoietic (CD34/CD45) or pluripotency (Nanog, Oct4) markers. Hyperglycaemia significantly increased CFEs at PD50 and PD100, which decreased at PD200. CB-MSC osteogenic differentiation was also inhibited by hyperglycaemia at PD15, PD100 and PD200, but not at PD50. Hyperglycaemia inhibited CB-MSC adipogenic differentiation to a lesser extent at PD15 and PD50, with reduced adipogenesis overall at PD100 and PD200.
CONCLUSION: This study demonstrates the limited negative impact of hyperglycaemia on the proliferative and stem cell characteristics of heterogeneous CB-MSC populations, although minor sub-population(s) appear more susceptible to these conditions leading to impaired osteogenic/adipogenic differentiation capabilities. Such findings potentially highlight the impact of hyperglycaemia on CB-MSC bone repair capabilities in situ.
METHODS: A literature search was performed via PubMed and ScienceDirect from 2001 to 2022, using the keywords "neurotransmitter," "stem cell," "tooth regeneration," "tooth repair," "regenerative dentistry," and "dental pulp." Different inclusion/exclusion criteria were used, and the search was restricted to English articles.
RESULTS: Nine publications reporting neurotransmitter interactions with stem cells for tooth and pulp regeneration were selected.
CONCLUSION: Neurotransmitters were found to interact with dental stem cells. Evidence pointing to neurotransmitters as a factor in the increased proliferation of stem cells was found. This review thus gives hope for tooth pulp regeneration and repair.
Objectives: This study aimed at optimizing the composition of Ag-Al hydrogel beads and their dissolving agents for potential use in the transportation of stem cells.
Methods: Various agarose, alginate, and CaCl2 concentrations were tested to construct hydrogel beads. The degradation rate and swelling ratio of each hydrogel sample were recorded. The optimized Ag-Al hydrogels were used for encapsulation of stem cells from human exfoliated deciduous teeth (SHED). Optimization of dissolving agents was performed and tested with the hydrogel-encapsulated cells. Data were statistically analyzed in SPSS.
Results: The selected concentration of Ag-Al hydrogels components was successfully demonstrated to encapsulate SHED, which remained viable until day 10. An average of 2 min was required for degradation of the hydrogel with encapsulated SHED by a dissolving agent consisting of 100 mM sodium citrate and 100 mM EDTA. The cell viability of SHED released after day 10 of encapsulation was 29.1%.
Conclusion: Alteration of Ag-Al components has considerable influence on the mechanical properties of the constructed hydrogel. The feasibility of performing the optimized cell encapsulation protocol, as well as the dissolving step, may provide a useful guide for the transportation of viable cells between countries, for medical research.
METHODS: Electronic databases were searched for studies investigating IL-37 and SLE. Data on IL-37 levels, SLE Disease Activity Index (SLEDAI) score, genetic polymorphisms, and its therapeutic effects from pre-clinical studies were extracted.
RESULTS: Previous studies presented conflicting findings on IL-37 levels in SLE patients. Some reported positive correlations with disease activity, while others observed associations between lower IL-37 and increased activity. Genetic variations in the IL-37 gene linked to SLE susceptibility have been reported. Pre-clinical studies using engineered mesenchymal stem cells or direct IL-37 treatment showed promise in reducing disease severity in mouse models and cell cultures of SLE. The analysis of multiple studies reveals that IL-37 expression varies significantly across different SLE subtypes.
CONCLUSIONS: While a potential link exists between IL and 37 and disease activity, genetic predisposition, and therapeutic benefit, further research is needed. Future studies with standardized designs, larger and more diverse populations, and mechanistic investigations are crucial to determine the therapeutic potential of IL-37 for SLE. This review highlights the need for well-designed clinical trials to evaluate the safety and efficacy of IL-37 therapy in patients with SLE.