Integrative analysis of the contribution of mRNAs and long non‑coding RNAs to the pathogenesis of asthma

Abstract

asthma, a common but poorly controlled disease, is one of the most serious health problems worldwide; however, the mechanisms underlying the development of asthma remain unknown. long non-coding rnas (lncrnas) and mrnas serve important roles in the initiation and progression of various diseases. The present study aimed to investigate the role of differentially expressed lncrnas and mrnas associated with asthma. differentially expressed lncrnas and mrnas were screened between the expression data of 62 patients with asthma and 43 healthy controls. Gene ontology (Go) and Kyoto encyclopedia of Genes and Genomes (KeGG) analyses were performed to investigate the biological functions and pathways associated with the lncrnas and mRNAs identified. Protein-protein interaction (PPI) networks were subsequently generated. in addition, lncrna-mrna weighted co-expression networks were obtained. in total, 159 differentially expressed lncrnas and 1,261 mrnas were identified. GO and KEGG analyses revealed that differentially expressed mrnas regulated asthma by participating in the 'vascular endothelial (VeGF) signaling pathway', 'oxidative phosphorylation', 'Fc ε ri signaling pathway', 'amino sugar and nucleotide sugar metabolism', 'histidine metabolism', 'β-alanine metabolism' and 'extracellular matrix-receptor interaction' (P<0.05). Furthermore, protein kinase B 1 had the highest connectivity degree in the PPi network, and was significantly enriched in the 'VEGF signaling pathway' and 'Fc ε ri signaling pathway'. a total of 8 lncrnas in the lncrna-mrna co-expression network were reported to interact with 52 differentially expressed genes, which were enriched in asthma-associated Go and KeGG pathways. The results obtained in the present study may provide insight into the profile of differentially expressed lncrnas associated with asthma. The identification of a cluster of dysregulated lncrnas and mrnas may serve as a potential therapeutic strategy to reverse the progression of asthma.

Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model

“…Disturbance of amino sugar and nucleotide sugar metabolism was found in hypertrophic cardiomyopathy 47 and asthma, a chronic inflammatory airway disease with the characteristic of airway remodeling. 48 N -acetyl- d -glucosamine 6-phosphate, an intermediate metabolite of amino sugar and nucleotide sugar metabolism, which was dysregulated both in PAs and the RV in our PAH model, was identified as a potential biomarker for the diagnosis of coronary heart disease (a kind of cardiovascular disease that was thought to undergo a metabolic shift). 49 Taken together, our results suggested that the perturbation of energy metabolism was involved in the development of flow-associated PAH, especially the carbohydrate metabolism.…”

The Identification of Childhood Asthma Progression-Related lncRNAs and mRNAs Suitable as Biomarkers Using Weighted Gene Coexpression Network Analysis

“…Furthermore, Dolcino et al [ 13 ] analyzed the transcript profiles of rheumatoid arthritis (RA) patients and healthy donors and found that lncRNA RP11-4989.15 plays an important role in RA pathogenesis. Another study screened eight important lncRNAs interacting with 52 differentially expressed genes enriched in asthma-associated pathways, and these lncRNAs have the potential to serve as underlying biomarkers useful for the future development of therapeutic strategies [ 14 ]. Nevertheless, specific biomarkers for childhood asthma have not been identified, and the roles of lncRNAs in childhood asthma remain unclear.…”

LncRNA MORT (ZNF667-AS1) in Cancer—Is There a Possible Role in Gynecological Malignancies?

“…A bioinformatics study using gene ontology and KEGG enrichment analysis of genes shows that, in asthmatic patients, the level of ZNF667-AS1 is downregulated when compared to healthy controls. This suggests that it may play a role in the pathogenesis of asthma [23]. ZNF667-AS1 was found to be upregulated in the plasma of patients with myocardial infarction when compared with healthy controls.…”