Gene Expression Profiling of Pulmonary Artery in a Rabbit Model of Pulmonary Thromboembolism

• Published in: PloS one Vol. 11; no. 10; p. e0164530
• Main Authors: Tang, Zhiyuan, Wang, Xudong, Huang, Jianfei, Zhou, Xiaoyu, Xie, Hao, Zhu, Qilin, Huang, Minjie, Ni, Songshi
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 31-10-2016; Public Library of Science (PLoS)
• Subjects: Analysis; Angina pectoris; Animal models; Animals; Arteries; Biology and Life Sciences; Biomarkers; Blood clots; Cardiovascular disease; Cardiovascular diseases; Catheters; Chemokines; Chronic obstructive pulmonary disease; Computational Biology - methods; Coronary vessels; Disease Models, Animal; Embolisms; Endothelium; Gene expression; Gene Expression Profiling; Gene Expression Regulation; Gene Regulatory Networks; Genes; Genomes; Health risk assessment; Heart diseases; Hospitals; Immunological diseases; Inflammation; Interleukin 8; Iodine; Laboratories; Lung diseases; Medical research; Medicine; Medicine and Health Sciences; Model accuracy; Mortality; Pathogenesis; Pulmonary arteries; Pulmonary artery; Pulmonary Artery - metabolism; Pulmonary Artery - pathology; Pulmonary Embolism - genetics; Pulmonary Embolism - pathology; Pulmonary hypertension; Rabbits; Reproducibility of Results; Research and Analysis Methods; Respiratory tract diseases; Signal Transduction; Signaling; Therapeutic applications; Thromboembolism; Thrombosis; Transcription; Transcriptome; Tumor necrosis factor-α; China
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0164530

Acute pulmonary thromboembolism (PTE) refers to the obstruction of thrombus in pulmonary artery or its branches. Recent studies have suggested that PTE-induced endothelium injury is the major physiological consequence of PTE. And it is reasonal to use PTE-induced endothelium injury to stratify disease severity. According to the massive morphologic and histologic findings, rabbit models could be applied to closely mimic the human PE. Genomewide gene expression profiling has not been attempted in PTE. In this study, we determined the accuracy of rabbit autologous thrombus PTE model for human PTE disease, then we applied gene expression array to identify gene expression changes in pulmonary arteries under PTE to identify potential molecular biomarkers and signaling pathways for PTE. We detected 1343 genes were upregulated and 923 genes were downregulated in PTE rabbits. The expression of several genes (IL-8, TNF-α, and CXCL5) with functional importance were further confirmed in transcript and protein levels. The most significantly differentially regulated genes were related to inflammation, immune disease, pulmonary disease, and cardiovascular diseases. Totally 87 genes were up-regulated in the inflammatory genes. We conclude that gene expression profiling in rabbit PTE model could extend the understanding of PTE pathogenesis at the molecular level. Our study provides the fundamental framework for future clinical research on human PTE, including identification of potential biomarkers for prognosis or therapeutic targets for PTE.