Chronic obstructive pulmonary disease: A crosstalk on nucleotide compositional dynamics and codon usage patterns of the genes involved in disease.
Nath Durbba,Deka Himangshu,Uddin Arif,Chakraborty Supriyo
Journal of cellular biochemistry
Chronic obstructive pulmonary disease (COPD), a lung disease, affects a large number of people worldwide, leading to death. Here, we analyzed the compositional features and trends of codon usage of the genes influencing COPD to understand molecular biology, genetics, and evolutionary relationships of these genes as no work was reported yet. Coding sequences of COPD genes were found to be rich in guanine-cytosine (GC) content. A high value (34-60) of the effective number of codons of the genes indicated low codon usage bias (CUB). Correspondence analysis suggested that the COPD genes were distinct in their codon usage patterns. Relative synonymous codon usage values of codons differed between the more preferred codons and the less-preferred ones. Correlation analysis between overall nucleotides and those at third codon position revealed that mutation pressure might influence the CUB of the genes. The high correlation between GC12 and GC3 signified that directional mutation pressure might have operated at all the three codon positions in COPD genes.
Whole transcriptome analyis of human lung tissue to identify COPD-associated genes.
Zhu Yizhang,Zhou Aiyuan,Li Qiuyu
Identification of the dysfunctional genes in human lung from patients with Chronic obstructive pulmonary disease (COPD) will help understand the pathology of this disease. Here, using transcriptomic data of lung tissue for 91 COPD cases and 182 matched healthy controls from the Genotype-Tissue Expression (GTEx) database. we identified 1359 significant differentially expressed genes (DEG) with 707 upregulated and 602 downregulated respectively. We evaluated the identified DEGs in an independent microarray cohort of 219 COPD and 108 controls, demonstrating the robustness of our result. Functional annotation of COPD-associated genes highlighted the activation of complement cascade, dysregulation of inflammatory response and extracellular matrix organization in the COPD patients. In addition, we identified several novel key-hub genes involved in the COPD pathogenesis using a network analysis method. To our knowledge, our analysis is currently the largest RNA-seq based COPD transcriptomic analyses, providing great resource for the molecular research in the COPD community.