Identification of significantly different modules between permanent and deciduous teeth by network and pathway analyses

Abstract

The differences in genetic backgrounds between deciduous and permanent teeth might contribute to the differences in developmental processes, histological characteristics, and tooth life cycles. Here, we attempted to identify significantly different modules between permanent and deciduous teeth via network and pathway analyses. We identified 291 differentially expressed genes (DEGs) between permanent and deciduous teeth using significance analysis of microarray methods. Co-expression networks of DEGs were constructed by weighted gene co-expression network analysis (WGCNA). Three pathways with a significant number of DEGs and P value <0.01 were identified. Integrated co-expression network and pathway (pathway and adjacent gene) analyses were used to extract three pathway-related modules: the calcium signaling pathway-related, ECM-receptor interaction pathway-related, and neuroactive ligand-receptor interaction pathway-related modules. We also attempted to analyze the topological centralities (degree, closeness, stress, and betweenness) of co-expression networks and modules. Four genes (TMEM229A, PPAPDC1A, LEPREL1, and GAD1) and three pathway-related modules that were significantly different in the deciduous and permanent teeth showed similar properties and good centralities. The relative expression levels of key genes were validated, and the differential expression of TMEM229A, LEPREL1, and GAD1 was confirmed by reverse transcription-polymerase chain reaction (P < 0.05). In conclusion, the results of this study may provide a greater understanding of the molecular pathogenesis and potential biomarkers of the progression from deciduous to permanent teeth.

Time-Dependent Response of Human Deciduous Tooth-Derived Dental Pulp Cells Treated with TheraCal LC: Functional Analysis of Gene Interactions Compared to MTA

“…Regarding neuroactive ligand-receptor interaction, this pathway can affect several aspects of cell behaviors. This pathway regulates tooth morphogenesis during tooth development [35]. A previous animal study with Raptor/mTORC1 knockout mice revealed that the animals presented less dentinogenesis [36].…”

Clinical significance of TMEM229A Q200del mutation in lung adenocarcinoma

“…Interestingly, we observed TMEM229A Q200del mutation was existed only in lepidic lung adenocarcinoma, but not in micropapillary lung adenocarcinoma, which was rstly identi ed. Previous report showed that downregulated expression of TMEM229A contributed to the progression from deciduous to permanent teeth [47]. In addition, Our previous study had con rmed that TMEM229A was lowly expressed in NSCLC and partly suppressed the NSCLC progression through inactivating the ERK pathway, suggesting TMEM229A was a suppressor gene in the development and progression of NSCLC [31].…”

TMEM229A suppresses non‑small cell lung cancer progression via inactivating the ERK pathway

“…TMEM229A is a seven-transmembrane protein with poorly defined biology. At present, research has revealed that TMEM229A serves a critical role in the development and differentiation of teeth ( 47 ). However, the current understanding of the expression and possible mechanism of TMEM229A is lacking, particularly with regard to that in cancer.…”