ISSN: 1449-1907International Journal of Medical Sciences
Global reach, higher impact
Int J Med Sci 2012; 9(5):380-386. doi:10.7150/ijms.4641 This issue Cite
Research Paper
Analysis on the Pathogenesis of Symptomatic Pulmonary Embolism with Human Genomics
1. Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China;
2. Department of Hematology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China;
3. Department of Laboratory Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China;
4. Department of Emergency, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
* Contributed equally.
Abstract
BACKGROUND: In the present study, the whole human genome oligo microarray was employed to investigate the gene expression profile in symptomatic pulmonary embolism (PE).
METHODS: Twenty patients with PE and 20 age and gender matched patients without PE as controls were enrolled into the present study in the same period. The diagnosis of PE was based on the clinical manifestations and findings on imaging examinations. Acute arterial and/or venous thrombosis was excluded in controls. The whole human genome oligo microarray was employed for detection. Statistical analysis was performed with t test following analysis of very small samples of repeated measurements and Gene Ontology (GO) analysis.
RESULTS: Genomic data showed no damage to vascular endothelial cells in PE patients. Genomic data only found increased mRNA expression of a small amount of coagulation factors in PE patients. In the PE group, anticoagulant proteins, Fibrinolytic system and proteins related to platelet functions only played partial roles in the pathogenesis of PE. In addition, the mRNA expressions of a fraction of adhesion molecules were markedly up-regulated. Gene Ontology analysis showed the genes with down-regulated expressions mainly explain the compromised T cell immunity. Symptomatic VTE patients have compromised T cell immunity.
CONCLUSION: The damage to vascular endothelial cells is not necessary in the pathogenesis of VTE, and only a fraction of factors involved in the shared coagulation cascade are activated. Genomic results may provide a new clue for clinical diagnosis, treatment and prevention of VTE.
Keywords: Human genomics, Pulmonary embolism (PE), T cell immunity, Adhesion molecules
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