[Temporal and spatial expression of Swell1 gene in the development of mouse condyle cartilage].

PURPOSE: To explore the temporal and spatial expression pattern of Swell1 (LRRC8A) gene in mouse condylar cartilage. METHODS: By obtaining condyle samples of embryos at 15.5, 16.5, 18.5 days and newborn mice, H-E staining, immunofluorescence staining and qRT-PCR were used to explore the microstructure of mouse condyles and the temporal and spatial expression changes of genes related to cartilage development and Swell1 gene. Statistical analysis was performed using SPSS 25.0 software package. RESULTS: Swell1 gene expression began in the hypertrophic chondrocyte layer during the development of the condyle from embryonic day 16.5, and then gradually increased, and continued to be expressed during mouse embryonic development until the mouse was born. CONCLUSIONS: Swell1 is mainly expressed in hypertrophic chondrocytes during the development of mouse condyles, and it may be involved in the regulation of chondrocyte hypertrophy.

p75 neurotrophin receptor positive dental pulp stem cells: new hope for patients with neurodegenerative disease and neural injury.

Neurodegenerative diseases and neural injury are 2 of the most feared disorders that afflict humankind by leading to permanent paralysis and loss of sensation. Cell based treatment for these diseases had gained special interest in recent years. Previous studies showed that dental pulp stem cells (DPSCs) could differentiate toward functionally active neurons both in vitro and in vivo, and could promote neuranagenesis through both cell-autonomous and paracrine neuroregenerative activities. Some of these neuroregenerative activities were unique to tooth-derived stem cells and superior to bone marrow stromal cells. However, DPSCs used in most of these studies were mixed and unfractionated dental pulp cells that contain several types of cells, and most were fibroblast cells while just contain a small portion of DPSCs. Thus, there might be weaker ability of neuranagenesis and more side effects from the fibroblast cells that cannot differentiate into neural cells. p75 neurotrophin receptor (p75NTR) positive DPSCs subpopulation was derived from migrating cranial neural crest cells and had been isolated from DPSCs, which had capacity of differentiation into neurons and repairing neural system. In this article, we hypothesize that p75NTR positive DPSCs simultaneously have greater propensity for neuronal differentiation and fewer side effects from fibroblast, and in vivo transptantation of autologous p75NTR positive DPSCs is a novel method for neuranagenesis. This will bring great hope to patients with neurodegenerative disease and neural injury.

Dlx2 over-expression: a possible mechanism for first branchial arch malformation.

The first branchial arch malformation (FBAM) is a rare congenital defect associated with anomalous development of the first and second branchial arches. Cause of FBAM still remains unknown, and is thought in most cases to be multifactorial, involving both genetic and enviromental factors. Dlx2 as a member of the Dlx homeobox gene family, plays a crucial role in the development of the first branchial arch. The tissues regulated mainly by Dlx2 are coincident with the tissues mainly involved in FBAM. Dlx2 over-expression generated by electroporation transfection can disturb the migration and differentiation of cranial neural crest cells (CNCCs), which migrate to the branchial arches and in turn give rise to much of the facial skeleton and connective tissues. Furthermore, Dlx2 over-expression can be found in the first branchial arch spontaneous mutant mice. So we hypothesize that Dlx2 over-expression mutation causes FBAM due to an increase in cell-cell adhesion and inhibiting the migration of CNCC to the first branchial arch in the early stage, or migrating to an incorrect position and can't differentiate into normal tissues. What an exact role of Dlx2 over-expression in FBAM remains to be investigated and Dlx2 over-expression transgenic mouse will be a nice model for further research in FBAM.