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Published on: August 4, 2021
Bioinformatics-Based Identification of Platelet-Related Genes and Analysis of Immune Infiltration Landscape in
Background:
Endometriosis is an estrogen-dependent inflammatory disease that is the leading cause of dysmenorrhea, infertility, and pelvic pain in women. A growing body of evidence has demonstrated that platelets may play an important role in its pathophysiology. Therefore, using bioinformatics analysis, we sought to determine the possible role of platelet-related genes in endometriosis and immune infiltration.
Methods:
GSE7305 and GSE51981 were used to identify differentially expressed genes (DEGs) in endometriosis. By crossing DEGs with platelet-related genes, the platelet-related DEGs were screened. Functional enrichment analyses were conducted. Then, the hub genes were identified using two machine algorithms, and receiver operating characteristic (ROC) curves were generated. Finally, the immune infiltration landscape and its connection with hub genes in endometriosis were assessed.
Results:
Six platelet-related hub genes (CD40, CSRP1, FLNA, C1GALT1C1, EIF2AK1, and PTMA) were screened out, and these genes showed high diagnostic specificity for endometriosis. Most immune cells exhibited higher infiltration levels in endometriosis. The abundance of activated B cells, myeloid-derived suppressor cells (MDSCs), macrophages, mast cells, monocytes, natural killer (NK) cells, neutrophils, T follicular helper cells, and type 1 T helper (Th1) cells in the endometriosis group was significantly higher than that in the control group, while activated CD4 T cells and immature dendritic cells were considerably less abundant. Correlation analysis revealed a link between hub genes and immune infiltration.
Conclusions:
Six hub platelet-related genes were identified and correlated with immune infiltration in endometriosis. Our research suggested that platelets may regulate the immune microenvironment of the endometriosis through signaling pathways involved in these genes, thereby contributing to its development and progression of endometriosis. These findings increase our understanding of endometriosis and may provide promising targets for disease treatment.
