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Bioinformatics analysis of molecular mechanisms of chronic obstructive pulmonary disease.
OBJECTIVE: This study was designed to explore the molecular mechanisms of Chronic Obstructive Pulmonary Disease (COPD) with DNA Microarray.
MATERIALS AND METHODS: The gene expression profile GSE475 was downloaded from Gene Expression Omnibus (GEO) database. There were 7 tissue samples of human diaphragm muscle available, including 4 normal samples and 3 samples from COPD patients. The differentially expressed genes (DEGs) were identified by LIMMA package in R language and were further analyzed using bioinformatics methods. Firstly, DEGs were classified into different COG clusters by BLAST. Then, the protein-protein interaction (PPI) network was constructed by STRING and pathways of DEGs were analyzed by FuncAssociate. Finally, the DEGs enriched diseases were obtained by EASE.
RESULTS: We selected 524 DEGs including 118 down-regulated DEGs and 406 up-regulated DEGs. The most significant pathway was JAK/STAT signaling pathway and the DEGs of IL6 and SOCS3 were directly participated in this pathway. Furthermore, the DEGs of SOCS3, IL4, IL18R1, IL1R1, and IL6 were participated in the disease of pulmonary fibrosis.
CONCLUSIONS: Our findings suggest that IL6 and SOCS3 play important roles in COPD and have the potential to serve as therapeutic targets of COPD.
MATERIALS AND METHODS: The gene expression profile GSE475 was downloaded from Gene Expression Omnibus (GEO) database. There were 7 tissue samples of human diaphragm muscle available, including 4 normal samples and 3 samples from COPD patients. The differentially expressed genes (DEGs) were identified by LIMMA package in R language and were further analyzed using bioinformatics methods. Firstly, DEGs were classified into different COG clusters by BLAST. Then, the protein-protein interaction (PPI) network was constructed by STRING and pathways of DEGs were analyzed by FuncAssociate. Finally, the DEGs enriched diseases were obtained by EASE.
RESULTS: We selected 524 DEGs including 118 down-regulated DEGs and 406 up-regulated DEGs. The most significant pathway was JAK/STAT signaling pathway and the DEGs of IL6 and SOCS3 were directly participated in this pathway. Furthermore, the DEGs of SOCS3, IL4, IL18R1, IL1R1, and IL6 were participated in the disease of pulmonary fibrosis.
CONCLUSIONS: Our findings suggest that IL6 and SOCS3 play important roles in COPD and have the potential to serve as therapeutic targets of COPD.
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