Background: Mesenchymal stromal cells (MSC) have the potential for self-renewal and differentiation in different tissues, characteristics that encourage their use in regenerative medicine. Dental tissue MSCs are easy to collect, have the same embryonic origin as neurons and have neuronal markers that allow their use in treating neurodegenerative diseases. Human exfoliated deciduous teeth (SHED)-derived stromal cells are considered immature and present positive expression of pluripotency and neuronal markers. Studies have shown that after induction of neuronal differentiation in vitro, SHED increased the expression of neuronal markers such as βIII-tubulin, Nestin, GFAP, NeuN, and NFM, demonstrating the potential use of these cells in preclinical studies. The results of this review reflect the consensus that in diseases such as spinal cord injury, cerebral ischaemia, and Alzheimer’s and Parkinson’s disease, SHED could function in the suppression of the inflammatory response, neuroprotection, and neuronal replacement. Conclusion: For these cells to be used in large-scale clinical trials, standardization of the isolation techniques and the neuronal induction medium used are necessary. The potential of SHED to induce neuronal differentiation is evident, demonstrating that this resource is promising and shows great potential for use in future preclinical and clinical trials of neurodegenerative diseases.
Objective: This study aimed to evaluate neuronal markers in stromal cells from human exfoliated deciduous teeth (SHED) and standardize the isolation and characterization of those cells. Methodology: Healthy primary teeth were collected from children. The cells were isolated by enzymatic digestion with collagenase. By following the International Society for Cell and Gene Therapy (ISCT) guidelines, SHED were characterized by flow cytometry and differentiated into osteogenic, adipogenic, and chondrogenic lineages. Colony-forming unit-fibroblasts (CFU-F) were performed to assess these cells’ potential and efficiency. To clarify the neuronal potential of SHED, the expression of nestin and βIII-tubulin were examined by immunofluorescence and SOX1, SOX2, GFAP, and doublecortin (DCX), nestin, CD56, and CD146 by flow cytometry. Results: SHED showed mesenchymal stromal cells characteristics, such as adhesion to plastic, positive immunophenotypic profile for CD29, CD44, CD73, CD90, CD105, and CD166 markers, reduced expression for CD14, CD19, CD34, CD45, HLA-DR, and differentiation in three lineages confirmed by staining and gene expression for adipogenic differentiation. The average efficiency of colony formation was 16.69%. SHED expressed the neuronal markers nestin and βIII-tubulin; the fluorescent signal intensity was significantly higher in βIII-tubulin (p<0.0001) compared to nestin. Moreover, SHED expressed DCX, GFAP, nestin, SOX1, SOX2, CD56, CD146, and CD271. Therefore, SHED had a potential for neuronal lineage even without induction with culture medium and specific factors. Conclusion: SHEDs may be a new therapeutic strategy for regenerating and repairing neuronal cells and tissues.
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