BACKGROUND:Development of neural crest cels, which is regulated by various genes, plays an important role in the formation of central nervous system, heart, craniofacial organs and other tissues. However, the relationship among these genes is unclear. OBJECTIVE:To investigate the molecular regulatory networks involved in the process of neural crest cel development based on a bioinformatic analysis. METHODS:Totaly 500 differentialy expressed genes during the process ofneural crest cel development were obtained from the GEO on-line database. Then the DAVID and STRING on-line databases were used to evaluate the relationship among these genes. RESULTS AND CONCLUSION:Totaly 500 differentialy expressed genes during theprocess of neural crest cel development could be enriched into different subgroups based on the analysis of DAVID database, including “transforming growth factor β signal pathway”, “WNT signal pathway”, “homeobox gene” , “neural crest cel differentiation” and “neural tube development”. Additionaly, 12 genes molecular networks were built based on the analysis of STRING database, such as DLX5, MSX2, SNAIL2, PAX7, SHH, SOX9, NOG, GSC, KAL1, bone morphogenetic protein 5, fibroblast growth factor 8 and WNT3a.These genes exhibited interactions by co-expression, activation and antagonism. Therefore, many genes involved in the process of neural crest cel development were interacted and formed the networks. These findings imply that we should understand these neural crest-related diseases from a holistic view of the signaling pathway and molecular regulatory networks.

Objective To observe the effect ofYinqiao Powder on the mouse models with upper respiratory trace mucosal immunity dysfunction infected with influenza virus A, and explore mechanism of action.Methods The mouse models of upper respiratory trace mucosal immunity dysfunction induced by cold stimulation with the influenza A/PR/8/34 (H1N1) virus through the nasal cavity were established. The mice were randomly divided into normal group, model group, positive medicine (Ribavirin) group, andYinqiao Powder group. All administration groups received gavage with relevant medicine, and then mortality, the life prolonging rate, average survival time and the lung index of each group were observed.Results Compared with the model group, the mortalities in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), with longer survival time. The lung indexes in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), and the inhibition ratios of lung index were 35.5% and 24.6%, respectively.ConclusionYinqiao Powder can realize the protective effects on upper respiratory infection through upregulating the mucosal immunity of the upper respiratory tract of mouse models.

Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues. Magnesium has been proved to promote bone healing under normal conditions. Here, we elucidate the mechanism by which Mg²⁺ promotes angiogenesis and osseointegration in diabetic status. We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised, with significantly decreased angiogenesis. We then developed Mg-coating implants with hydrothermal synthesis. These implants successfully improved the vascularization and osseointegration in diabetic status. Mechanically, Mg²⁺ promoted the degradation of Kelch-like ECH-associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells, thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia. Altogether, our data suggested that Mg²⁺ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.
Mice ; Animals ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Magnesium/metabolism* ; Osseointegration ; Diabetes Mellitus, Experimental/metabolism* ; Endothelial Cells/metabolism* ; NF-E2-Related Factor 2/metabolism*