Identifications of Molecular Makers for parathyroid hormone-releasing cell differentiation of tonsil-derived mesenchymal stem cells

Abstract

Background & Aim Introduction We previously reported that differentiated tonsil-derived mesenchymal stem cells embedded in matrigel restore parathyroid cell functions in rats with parathyroidectomy. We found that T-MSC are likely to differentiate into an endodermal lineage, in particular including parathyroid gland like cells (Biomaterial, 2015) These initial studies demonstrate that we can induce the expression of definitive parathyroid cell markers (GCM2, CASR, CCL21, and PTH) However, to be clinically applicable, this process must be conformed tonsil-derived mesenchymal stem cells to create cells for replacement of parathyroid function. Methods, Results & Conclusion Methods We analyzed transcriptomes using microarrays and then performed large-scale expression profiling of T-MSCs compared with undifferentiated T-MSCs and differentiation of 7days for parathyroid-like cells. Quantitative real-time polymerase chain reactions were performed to determine the mRNA levels. Results Using quantitative real-time RT-PCR the results were clearly confirmed. Comparing between control and differentiated parathyroid-like cells was different to expression of SCL7A14 (solute carrier family 7, member 14), AMOT (angiomotin), FGL2 (fibrinogen-like 2), and JUNB (jun B proto-oncogene). No correlation of Parathyroids cells was these genes, with Activin A and Shh treatments of cells and these genes were negative selection markers. Control cells increased fold change values, but differentiated parathyroid-like cells decreased fold change. Also control cells decreased fold change values and parathyroid-like cells decreased genes of HAPLN1 and INHBA. Conclusion The candidate genes identified as associated with parathyroid differentiation and by measuring the gene expression of multiple markers of target and nontarget cell types