Abstract
COPD is the fourth leading cause of mortality, and is predicted to be the third leading cause of death worldwide by 2020. But few studies on Tibetan COPD of China. This study identifies distinctive miRNA signatures in Tibetan COPD patients from Tibetan healthy subjects that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. In this study, a total of 210 differentially expressed miRNAs were screened. Analysis of the functions of target genes of differentially expressed miRNAs via GO enrichment analysis revealed that they mainly influenced guanyl-nucleotide exchange factor activity, cell morphogenesis and the positive regulation of GTPase activity. KEGG pathway enrichment analysis showed that these target genes were mainly enriched in signaling by NGF, Axon guidance, developmental biology, ubiquitin mediated proteolysis, and PDGF signaling pathways. MiR-106-5p and miR-486-5p expression was validated in the complete cohort. Age, plasma miR-106-5p, miR-486-5p, SP-D protein levels, and SP-D mRNA level were also determined to be correlated with FEV1%Pred, and may as the risk factors of Tibetan COPD. The combination of plasma miR-106-5p, miR-486-5p and SP-D mRNA expression may be the best model to assist the diagnosis of Tibetan COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) is an incompletely reversible, preventable, and treatable disease with airflow limitation characterized by high morbidity and mortality worldwide
Thirty-five Tibetan patients with COPD and Thirty-five Tibetan healthy people were included in this study as validation study
The present study aimed to identify the involvement of miRNAs and surfactant protein in the pathophysiology of COPD and to explore their effects with significant alteration on Tibetan COPD in vitro
Summary
Chronic obstructive pulmonary disease (COPD) is an incompletely reversible, preventable, and treatable disease with airflow limitation characterized by high morbidity and mortality worldwide. The complicated interaction between genetics, protein synthesis, and immune response in COPD is even more intricate when miRNAs regulation is introduced. These small noncoding RNAs are implicated in the immune response of C OPD5. They act by negatively regulating the expression of key immune development genes, contributing important logic elements to the regulatory circuitry. It has already been reported that differentially expressed miRNAs between healthy and COPD patients participated in organelle fission, inflammatory processes, and airway remodeling of COPD9,10.
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