Expression and role of interleukin‑1β and associated biomarkers in deep vein thrombosis

Abstract

Lower extremity deep vein thrombosis (DVT) is a common peripheral vascular disease, in which inflammation plays an important role. The aim of the present study was to investigate the expression and role of inflammatory factors in DVT. A rat model of venous thrombosis of the lower extremities was established through venous ligation surgery. The rats were examined at 2, 8, 24, 48 and 72 h after the induction of inferior venous stenosis and compared with control and sham surgery groups. The serum levels of interleukin-1β (IL-1β), tissue factor (TF) and xanthine oxidase (XOD) were measured using ELISAs. The morphology of the DVT tissue was observed by hematoxylin and eosin staining. Circulating endothelial cells (CECs) in peripheral blood were counted by flow cytometry. Reverse transcription-quantitative PCR and western blotting were used to detect mRNA and protein expression, respectively. The serum levels of IL-1β, TF and XOD exhibited no significant differences between the control and sham surgery groups. However, those in the rat model of DVT presented an upward trend from 2 to 24 h and peaked at 24 h, with a significant difference from the respective levels in the control and sham surgery groups. The histopathological analysis revealed the presence of red and mixed thrombi in the rats 2-48 h following the induction of inferior venous stenosis group with inflammatory cell infiltration in the vascular wall. Thrombus formation was evident after 72 h. While significant difference was observed in the number of CECs in the peripheral blood between the control and sham surgery groups, the number of peripheral blood CECs in the rats with inferior venous stenosis group increased from 8 to 72 h, with significant differences among these groups. The mRNA levels of IL-1β, TF, XOD and NF-κB in the tissues peaked at 24 h, with significant differences compared with those in the control and sham surgery groups. In addition, the protein expression level of NF-κB increased from 2 to 72 h. In conclusion, these results suggest that the high expression of IL-1β, TF, XOD and NF-κB may promote thrombus formation.

Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway

“…The apoptosis of HUVECs was inhibited by lncRNA XIST knockdown via miR-30c-5p/PTEN axis in atherosclerosis [ 39 ]. The TF level associated with dilated cardiomyopathy was improved through lncRNA XIST/miR-195-5p/NOVA1 axis [ 40 ], and the high level of TF facilitated thrombi formation in DVT patients [ 41 ].…”

Monocyte/macrophage-mediated venous thrombus resolution

“…IL-1β is one of the most prominent inflammatory mediators leading to fever and immune activation by binding to IL-1 receptor 1 ( 77 ). A previous study reported that serum IL-1β level and IL-1β mRNA expression increased in thrombus tissue at 24 h in a stasis rat model ( 78 ). However, it was not shown which cells in the thrombus IL-1β originates from ( 78 ).…”

Recent Advances on the Molecular Mechanism and Clinical Trials of Venous Thromboembolism

“… 23 Another study has demonstrated that elevated levels of inflammatory factors interleukin-1β (IL-1β), tissue factor (TF), xanthine oxidase (XOD) and nuclear factor kappa B (NF-κB) may accelerate thrombosis. 26 The NLRP3/IL-1/NF-κB signaling mechanisms regulate IL-1 and tumor necrosis factor alpha (TNF-α), which may be essential signs of the prethrombotic condition due to slowed blood flow, impaired vascular endothelium, and elevated tissue factor expression. Therefore, VTE is the result of the coagulation system’s cascade reaction.…”