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Objective: To first induce chronic deep venous thrombosis in the left iliac veins of canines and porcines and then compare these two models to validate endovascular treatment devices. Methods: Thrombin and fibrinogen were used to produce a solid thrombus in the left iliac veins of a stenosis model. The researchers used venous angiography and histological staining to investigate the progression of thrombosis. Results: A left iliac vein thrombus was successfully formed in all experimental animals, including six Labrador dogs and three Bama miniature pigs, and there was minimal surgical bleeding. All dogs survived until 90 days, and three pigs died on Days 29, 33, and 58. Conclusion: The researchers first established the models and then observed the progression of chronic deep venous thrombosis of the iliac vein in large animals for up to 90 days. Dogs are better suited for chronic deep venous thrombosis models due to their uncomplicated anatomy, excellent obedience, and proneness to physical activity compared with pigs. [ABSTRACT FROM AUTHOR]

Background: Endothelial progenitor cells (EPCs) contribute to recanalization of deep vein thrombosis (DVT). This study aimed to detect miRNA expression profiles in EPCs from patients with DVT and characterize the role of miRNA in EPCs dysfunction.Methods: EPCs was isolated from DVT patients and control subjects, and miRNA expression profiles were compared to screen differential miRNAs. The candidate miRNAs were confirmed by RT-PCR analysis. The targets of miRNA were identified by bioinformatics analyses, luciferase reporter assay and gene expression analyses. The apoptosis, migration and tube formation of EPCs were examined by flow cytometry, transwell assay and matrigel tube formation assay. A rat model of venous thrombosis was established as in vivo model.Results: We identified miR-483-3p as a candidate miRNA upregulated in EPCs from DVT patients. By using miR-483-3p agomir and antagomir, we demonstrated that miR-483-3p decreased the migration and tube formation while increased the apoptosis of EPCs. Moreover, we identified serum response factor (SRF) as the target of miR-483-3p, and showed that SRF knockdown decreased the migration and tube formation while increased the apoptosis of EPCs. In addition, miR-483-3p inhibition led to enhanced ability of homing and thrombus resolution of EPCs in rat model of venous thrombosis.Conclusions: miR-483-3p is upregulated in EPCs from DVT patients, and it targets SRF to decrease EPCs migration and tube formation and increase apoptosis in vitro, while decrease EPCs homing and thrombus resolution in vivo. MiR-483-3p is a potential therapeutic target in DVT treatment. [ABSTRACT FROM AUTHOR]