Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. This review focuses on the different stages of atherosclerosis development, ranging from endothelial dysfunction to plaque rupture. In addition, the post-transcriptional regulation and modulation of atheroma plaque by microRNAs and lncRNAs, the role of microbiota, and the importance of sex as a crucial risk factor in atherosclerosis are covered here in order to provide a global view of the disease.

/pdf/pathophysiology-of-atherosclerosis-1e29razn.pdf

Pathophysiology of Atherosclerosis

Thrombosis, the localized clotting of blood that affects arterial or venous circulation, is one of the leading causes of death worldwide.1 Currently used antithrombotic drugs have increased bleeding risk.2,3 Exploring new antithrombotic strategies that preserve physiological hemostasis is under intensive investigation. Classical triad of causative factors leading to thrombosis includes alterations in blood content, alterations in blood flow, and alterations in the vessel wall. Endothelium, the inner most single layer of cells lining the blood vessels, provides a surface for thrombosis formation and critically regulates blood fluidity and homeostasis. As barrier, endothelium separates blood clotting factors from exposure to subendothelial prothrombotic extracellular matrix components. Endothelium also secretes or expresses vasoactive factors that modulate platelet reactivity, coagulation, fibrinolysis, and vascular contractility, all of which contribute to thrombotic formation. Such factors include nitric oxide, prostacyclin, Von Willebrand factor (VWF), thrombomodulin, endothelin, etc. Accumulating evidences show that endothelial cells (ECs) play a pivotal role in modulating thrombosis, highlighting ECs as a potential target for thrombosis control. In this Recent Highlights, we reviewed recent publications in Arteriosclerosis, Thrombosis, and Vascular Biology and other leading journals that are focused on the mechanisms of endothelial regulation of thrombosis and discussed their merits in therapeutic discovery.

Arterial thrombosis is commonly initiated by vascular endothelial erosions and ruptures of an atherosclerotic plaque3,4 while venous thrombosis mainly stems from blood stasis.5 Despite these differences, platelet adhesion/activation, and fibrin deposition as the result of coagulation constitute the fundamental processes of thrombus formation.6,7 Platelet activation occurs when they interact with activated ECs (with increased VWF release and selectin expression) via glycoprotein Ib-V-IX complex binding to VWF, or when they expose to subendothelial extracellular matrix components, such as collagen (via glycoprotein VI receptor), in the cases of endothelial injury or plaques …

Thrombotic Regulation From the Endothelial Cell Perspectives.

MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at a post-transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis-related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA-based biomarkers in the diagnosis, treatment and prognosis of angiogenesis-related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jcmm.13700

The regulatory role of microRNAs in angiogenesis-related diseases.

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. 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. 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. 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.

/pdf/upregulation-of-mir-483-3p-contributes-to-endothelial-31t8eywjey.pdf

Upregulation of miR-483-3p contributes to endothelial progenitor cells dysfunction in deep vein thrombosis patients via SRF

// Yuan Qu 1, 2, * , Jing Wu 2, 3, * , Jia-Xin Deng 2 , Yu-Ping Zhang 2 , Wan-Yi Liang 2 , Zhen-Lan Jiang 2 , Qing-Hong Yu 2 , Juan Li 1, 3 1 Department of Internal Medicine of Traditional Chinese Medicine, College of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510510, Guangdong, P. R. China 2 Department of Rheumatology and Clinical Immunology, Zhujiang Hospital of Southern Medical University, Guangzhou 510282, Guangdong, P. R. China 3 Department of Rheumatology, Nanfang Hospital, Southern Medical University, Guangzhou 510510, Guangdong, P. R. China * These authors have contributed equally to this work Correspondence to: Juan Li, email: LIjuanLJ07@163.com Qing-Hong Yu, email: yuqinghonghome@163.com Keywords: microRNA-126, PIK3R2, PI3K-AKT, rheumatoid arthritis, synovial fibroblasts Received: April 14, 2016     Accepted: July 10, 2016     Published: October 06, 2016 ABSTRACT Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation and destruction of the joints as well as an increased risk of cardiovascular disease. RA synovial fibroblasts (RASFs) are involved in the progression of RA and release pro-inflammatory cytokines. On the other hand, microRNAs (miRs) may help control the inflammatory response of immune and non-immune cells. Therefore, our study used lentiviral expression vectors to test the effects of miR-126 overexpression on RASF proliferation and apoptosis. Luciferase experiments verified the targeting relationship between miR-126 and PIK3R2 gene. The co-transfection of anti-miR-126 and PIK3R2 siRNA to RASFs were used to identify whether PIK3R2 was directly involved in proliferation and apoptosis of miR-126-induced RASFs. Real-time polymerase chain reaction (PCR) was used to detect miR-126 and PIK3R2 expressions. MTT assay was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis and cell cycle. Western blotting was used to detect PIK3R2, PI3K, AKT and p-AKT proteins. After Lv-miR-126 infected RASFs, the relative expression of miR-126 was significantly enhanced. MiR-126 promoted RASF proliferation and inhibited apoptosis. Levels of PIK3R2 decreased while total PI3K and p-AKT levels increased in RASFs overexpressing miR-126. Co-transfection of anti-miR-126 and PIK3R2 siRNA also increased PI3K and p-AKT levels as well as RASF proliferation and reduced apoptosis, as compared to anti-miR-126 treatment alone. Finally, luciferase reporter assays showed that miR-126 targeted PIK3R2 . Our data indicate that miR-126 overexpression in RASFs inhibits PIK3R2 expression and promotes proliferation while inhibiting apoptosis. This suggests inhibiting miR-126 may yield therapeutic benefits in the treatment of RA.

/pdf/microrna-126-affects-rheumatoid-arthritis-synovial-101eq4aemj.pdf

MicroRNA-126 affects rheumatoid arthritis synovial fibroblast proliferation and apoptosis by targeting PIK3R2 and regulating PI3K-AKT signal pathway.

ObjectivesTo report *The first two authors contributed equally to this work.our clinical experience on diagnostic criteria and endovascular management in patients with iliac venous compression syndrome.MethodBetween July 2013 and May 2015, 85 consecutive patients with suspected iliac venous compression syndrome were evaluated by transfemoral venography and intravascular ultrasonography. Venographic evidence of iliac venous occlusion, stenosis, or pelvic collateral vessels, and the degree of stenosis as examined with intravascular ultrasonography were recorded. The endovascular procedure, complications, clinical outcome, and the Venous Clinical Severity Score were evaluated before and after the intervention.ResultsOf the 85 limbs, 66 cases of iliac venous compression syndrome were confirmed and 19 cases were excluded. In all of the 66 patients, we successfully performed endovascular intervention (22 balloon dilations, 44 balloon dilations + stenting). Two patients with stent implantation developed acute lo...

https://journals.sagepub.com/doi/pdf/10.1177/0268355518764989

Diagnosis and endovascular treatment of iliac venous compression syndrome.

Background: Preclinical and clinical studies indicated that endothelial progenitor cells (EPCs) enhanced blood vessel formation in many clinical situations. However, whether transplantation of EPCs would enhance chronic venous thrombus recanalization and resolution is unknown. Methods: Mononuclear cells were isolated from bone marrow of immature rats by density gradient centrifugation, cultured, and then transplanted into inferior vena cava of rats with experimentally induced thrombi. Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), messenger RNA (mRNA), and protein expression levels were measured through real-time quantitative polymerase chain reaction and Western blotting of thrombi and adjacent caval walls 14 days following transplantation. Results: Transplantation of bone marrow-derived EPCs led to an increase in VEGF, bFGF, mRNA, and protein expression. In addition, transplantation of bone marrow-derived EPCs also resulted in reduced thrombus size and increased neovas...

https://journals.sagepub.com/doi/pdf/10.1177/1076029610397180

Transplantation of ex vivo expanded bone marrow-derived endothelial progenitor cells enhances chronic venous thrombus resolution and recanalization.

Atherosclerosis is a sustained inflammatory disease of the arterial wall. The purpose of the current study is to investigate the effect of sodium ferulate on the proliferation and migration of human vascular smooth muscle cells (hVSMCs). In addition, we also sought to determine whether HMGB1 knockdown could potentiate the anti-inflammatory effects of sodium ferulate. hVSMCs were treated with oxidized lower-density lipoprotein (ox-LDL, 50 mg/l) to induce inflammation. Cells were then treated with sodium ferulate and HMGB1 silencing (SiHMGB1) individually or in combination. The phenotypes of the treated cells including proliferation, cell cycle profile, apoptosis, and gene expression were analyzed. Results showed that sodium ferulate or SiHMGB1 treatment inhibited ox-LDL-induced inflammation in hVSMCs. Furthermore, the combination of SiHMGB1 plus sodium ferulate treatment displayed an additive effect in inhibiting the proliferation and migration of hVSMCs. Consistently, the suppression of receptor for advanced glycation end products expression was also observed. ICAM-1 and transforming growth factor-β suggest that these signaling components were involved in the anti-inflammatory effect. Our study confirms the anti-inflammatory function of sodium ferulate, and uncovered the potentiating effect of HMGB1 knockdown in suppressing ox-LDL-induced proliferation and migration of hVSMCs. Inhibition of HMGB1 expression in addition to sodium ferulate treatment might be a more effective therapeutic approach for atherosclerosis.

HMGB1 Silencing Potentiates the Anti-inflammatory Effects of Sodium Ferulate in ox-LDL-Stimulated Vascular Smooth Muscle Cells

Objective
To evaluate the efficacy and safety of catheter-directed thrombolysis (CDT) in treating with inferior vena cava (IVC) thrombosis after filter implantation.


Methods
A retrospective analysis of 13 patients with IVC thrombosis after filter implantation was conducted at our institution from June 2009 to June 2012. A total of 26 lower extremities were involved. IVC filters were implanted via right internal jugular vein. Then CDT was performed through small saphenous vein, popliteal vein or femoral vein. The dosage of urokinase was 0.6-1 million/day. The occlusive segment in IVC was managed with percutaneous transluminal angioplasty (PTA) and stenting.


Results
The obstructed IVC was re-opened after CDT in 11 cases. The average CDT time was 8.3 (7-13) days. PTA (n=2) and stenting (n=1) were performed. A total of 4 retrievable filters were planted and retrieved later successfully. No severe complications occurred. During the follow-ups, no clinically detetable sighs of pulmonary embolism were observed.


Conclusion
CDT is effective, safe and feasible in the treatment of IVC thrombosis after filter implantation.


Key words: 
Inferior vena cava; Thrombosis; Filter; Catheter-directed thrombolysis

[Therapy of catheter-directed thrombolysis for inferior vena cava thrombosis after filter implantation].

WITHDRAWN: Advances in the research of a novel mode of the Vascular Epidermal Growth Factor Receptor tyrosine kinase inhibitors

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