Editor's Choice - Clinical Efficacy of Venastent - A Novel Iliac Vein Stent for Non-Thrombotic Iliac Vein Lesions: A Multi-Centre Randomised Controlled Trial.

OBJECTIVE: To determine the efficacy of Venastent - a novel iliac vein stent for non-thrombotic iliac vein lesions (NIVLs). METHODS: From October 2018 to January 2021, 256 NIVL patients were recruited at 19 Chinese hospitals. A randomised controlled trial was conducted to compare the efficacy of the new iliac vein stent-Venastent (Tianhong China) with Zilver stent (Cook USA). All patients were allocated randomly to two groups: the experimental group patients used Venastent, while the control group received the Zilver stent. The trial was registered in Chinese Clinical Trial Registry (ChiCTR2200057851). RESULTS: A total of 123 patients in the experimental group and 122 patients in the control group had a full set of data collected (p = ns). The technical success rate was 100% (n = 245/245). The patency rate was 100% (n = 123/123) in the experimental group and 98.4% (n = 120/122) in control group one year after operation (p = ns). The lower extremity swelling remission rate was 79.1% (n = 87/110) in the experimental group and 78.4% (n = 91/116) in the control group (p = ns). The lower extremity pain relief rate was 68.8% (n = 50/80) in the experimental group and 77.2% (n = 71/92) in the control group (p = ns). The ulcer healing rate was 90% (n = 18/20) in the experimental group and 87% (n = 20/23) in the control group (p = ns). There was no difference in stent re-stenosis or clinical remission between the two groups. CONCLUSION: The new iliac vein stent, Venastent, had a comparable high patency rate and safety profile as the Zilver stent (Cook) in NIVLs patients. Venastent significantly reduced symptoms of chronic venous disease.

G protein-coupled receptor 39 activation alleviates oxidized low-density lipoprotein-induced macrophage inflammatory response, lipid accumulation and apoptosis by inducing A20 expression.

G protein-coupled receptor 39 (GPR39) agonist weakens oxidized low-density lipoprotein (ox-LDL)-induced attachment of monocytes to vascular endothelial cells and thus alleviates atherosclerosis. This study looks at whether GPR39 protects macrophages against ox-LDL-induced inflammation and apoptosis and ameliorates lipid accumulation in atherosclerosis and investigates its mechanism. Following inducement of ox-LDL, the expression of GPR39 and tumor necrosis factor alpha-induced protein 3 (TNFAIP3, also known as A20) in Raw 264.7 cells was detected by RT-qPCR and western blotting. The viability of macrophages treated with GPR39 agonist was detected by a cell counting kit 8 kit. GPR39 and A20 expression in ox-LDL-challenged macrophages was assayed by RT-qPCR and western blot with or without GPR30 agonist. After transfection of small interfering RNA (siRNA)-A20, the expression of pro-inflammatory cytokine tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6 and anti-inflammatory cytokine IL-10 as well as NF-κB p65 and COX2 was detected. Lipid accumulation was observed through Oil Red O Staining. Total cholesterol (TC) and free cholesterol (FC) in macrophages were detected by commercial kits. Lastly, macrophage apoptosis was observed through TUNEL, and apoptosis-related proteins were detected by western blotting . Results indicated that decreased expression of GPR39 and A20 was observed in ox-LDL-induced macrophages. GPR39 agonist significantly increased A20 expression in ox-LDL-treated macrophages. Furthermore, A20 interference reversed the inhibitory effect of GPR39 agonist on ox-LDL-induced inflammation, lipid accumulation, TC and FC overexpression as well as cell apoptosis. In conclusion, activating GPR39 alleviates ox-LDL-induced macrophage inflammation, lipid accumulation and apoptosis in an A20-dependent manner.

Characteristics of immunogenic and tolerogenic dendritic cells within the arterial wall in atherosclerosis and in vitro.

AIM: To investigate the characteristic of mature dendritic cell (mDC) and tolerogenic dendritic cell (TDC) in human lower limb atherosclerosis occlusion syndrome (ASO) and diabetic foot and in vitro. METHODS: 58 human ASO and diabetic foot arterial specimens were collected from surgical operation and autopsy. Immunohistochemical and Western blotting method were used to examine the distribution and the content of CD83 and CD1a positive reaction mDC and CD11b and DC-SIGN positive reaction TDC. Furthermore, bone marrow-derived DCs were induced by rmGM-CSF and rmIL-4 in the presence or absence of LPS in vitro. The percent of CD11c(+)CD11b(+)TDC and CD11c(+)CD83(+)mDC were analyzed by flow cytometry. The effects of TDC and mDC on T lymphocytes were analyzed by the IL-17 level, the percent of Th17, and IL-17 mRNA expression. RESULTS: Immunogenicity mDC was heavily found in intima plaque and around the small vessel of adventitia on artherosclerosis aorta of lesion group, and was positively correlated to the progress of the disease. However, there were low expression of TDC and was negatively correlated to the progress of the disease. Meanwhile, we found that there is a close relationship between high glucose and disease progression. TDC expressed high levels of IL-10 and TGF-ß1 and down-regulated the percent of CD4(+)IL-17(+) Th17, IL-17 mRNA and the level of IL-17 in vitro. CONCLUSION: TDC and mDC are assembled in the process of ASO, and the progression of the disease might be aggravated by DC-maturation. High glucose might closely relate to the progression of atherosclerosis.