Background: CD146 is a tight junction associated molecule involved in maintaining endothelial barrier and balancing immune-inflammation response in cardiovascular disease. Notably, the peripheral CD146+ cells significantly upsurge under vessel dyshomeostasis like acute myocardial injury (AMI), appearing to be promising therapeutic targets. In this study, in a new view of gene correlation, we aim at deciphering the underlying complex mechanism of CD146+ cells in the development of AMI.
Methods: Transcription dataset GSE 66360 of CD146+ blood cells from clinical subjects were downloaded from NCBI. Pearson networks were constructed and the clustering coefficients were calculated to disclose the differential connectivity genes (DCGs). Analysis of gene connectivity and gene expression was performed to reveal the hub genes and hub genes clusters followed by gene enrichment analysis.
Results and Conclusions: Among the total 23520 genes, 27 genes out of 126 differential expression genes are identified as DCGs. Those DCGs normally stay in the peripheral of networks while transfer to the functional central position under AMI situation. Moreover, it is revealed that DCGs spontaneously crowd together into two functional models, CCL20 cluster and NR4A3 cluster, influencing the CD146-mediated signaling pathways during the pathology of AMI for the first time.