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Engineering small-caliber vascular grafts from collagen filaments and nanofibers with comparable mechanical properties to native vessels.

At the present time, there is no successful synthetic, off-the-shelf small-caliber vascular graft (<6 mm) for the repair or bypass of the coronary or carotid arteries. This stimulates on-going investigations to fabricate an artificial vascular graft that has both sufficient mechanical properties as well as superior biological performance. Collagen has long been considered as a viable material to encourage cell recruitment, tissue regeneration, and revascularization, but its use has been limited by its inferior mechanical properties. In this study, novel electrochemically aligned collagen filaments were used to engineer a bilayer small-caliber vascular graft, by circular knitting the collagen filaments and electrospinning collagen nanofibers. The collagen prototype grafts showed significantly greater bursting strength under dry and hydrated conditions to that of autografts such as the human internal mammary artery and the saphenous vein (SV). The suture retention strength was sufficient under dry condition, but that under hydrated condition needs to be further improved. The radial dynamic compliance of the collagen grafts was similar to that of the human SV. During in vitro cell culture assays with human umbilical vein endothelial cells, the prototype collagen grafts also encouraged cell adhesion and promoted cell proliferation compared to the synthetic poly(lactic acid) grafts. In conclusion, this study demonstrated the feasibility of the use of novel collagen filaments for fabricating small caliber tissue-engineered vascular grafts that provide both sufficient mechanical properties and superior biological performance.

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Native Human Collagen V Native Influenza HA (A To Native Mouse Collagen I I Native Human Collagen I P Native Human Collagen IV Native Bovine Collagen II Native Influenza HA (A To Native Mouse Collagen I P Native Human Collagen II Native Influenza HA (A To Native Bovine Collagen II Native Human Collagen V A

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Behavior of Smooth Muscle Cells under Hypoxic Conditions: Possible Implications on the Varicose Vein Endothelium.

Varicose veins are a disease with high incidence and prevalence. In the venous wall, the smooth muscle cells (SMCs) act in the vascular homeostasis that secretes multiple substances in response to stimuli. Any alteration of these cells can modify the function and structure of the other venous layers such as the endothelium, resulting in increases in endothelial permeability and release of substances. Therefore, knowing the cellular and molecular mechanisms of varicose veins is imperative. The aims of this study are to understand how SMCs of patients with varicose veins subjected to saphenectomy of the great saphenous vein react under hypoxic cell conditions and to determine the role of vascular endothelial growth factor (VEGF) in this process. We obtained SMCs from human saphenous vein segments from patients with varicose veins (n=10) and from organ donors (n=6) undergoing surgery. Once expanded, the cells were subjected to hypoxic conditions in specific chambers, and expansion was examined through analyzing morphology and the expression of -actin. Further gene expression studies of HIF-1, EGLN3, VEGF, TGF-1, eNOS, and Tie-2 were performed using RT-qPCR. This study reveals the reaction of venous cells to sustained hypoxia. As significant differential gene expression was observed, we were able to determine how venous cells are sensitive to hypoxia. We hypothesize that venous insufficiency leads to cellular hypoxia with homeostatic imbalance. VEGF plays a differential role that can be related to the cellular quiescence markers in varicose veins, which are possible therapeutic targets. Our results show how SMCs are sensitive to hypoxia with a different gene expression. Therefore, we can assume that the condition of venous insufficiency leads to a situation of sustained cellular hypoxia. This situation may explain the cellular response that occurs in the venous wall as a compensatory mechanism.

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Monoclonal Anti Actin, β Anti-Actinin, smooth musc Anti-bodywall muscle cell Actin, Smooth Muscle Ab-1 RFP Expressing Human Umbi GFP Expressing Human Saph Monoclonal Anti-Actin, β Anti bodywall muscle cell GFP Expressing Human Umbi Goat Anti-Human, Mouse, R Monoclonal Anti Actin, β Anti-bodywall muscle cell

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Decellularization and Recellularization Methodology for Human Saphenous Veins.

Vascular conduits used during most vascular surgeries are allogeneic or synthetic grafts that often lead to complications caused by immunosuppression and poor patency. Tissue engineering offers a novel solution to generate personalized grafts with a natural extracellular matrix containing the recipient's cells using the method of decellularization and recellularization. We show a detailed method for performing decellularization of the human saphenous vein and recellularization by perfusion of peripheral blood. The vein was decellularized by perfusing 1% Triton X-100, 1% tri-n-butyl-phosphate (TnBP) and 2,000 Kunitz units of deoxyribonuclease (DNase). Triton X-100 and TnBP were perfused at 35 mL/min for 4 h while DNase was perfused at 10 mL/min at 37 °C for 4 h. The vein was washed in ultrapure water and PBS and then sterilized in 0.1% peracetic acid. It was washed again in PBS and preconditioned in endothelial medium. The vein was connected to a bioreactor and perfused with endothelial medium containing 50 IU/mL heparin for 1 h. Recellularization was performed by filling the bioreactor with fresh blood, diluted 1:1 in Steen solution, and adding endocrine gland-derived vascular endothelial growth factors (80 ng/mL), basic fibroblast growth factors (4 µL/mL), and acetyl salicylic acid (5 µg/mL). The bioreactor was then moved into an incubator and perfused for 48 h at 2 mL/min while maintaining glucose between 3 - 9 mmol/L. Later, the vein was washed with PBS, filled with endothelial medium and perfused for 96 h in the incubator. Treatment with Triton X-100, TnBP and DNase decellularized the saphenous vein in 5 cycles. The decellularized vein looked white in contrast to normal and recellularized veins (light red). The hematoxylin & eosin (H&E) staining showed the presence of nuclei only in normal but not in decellularized veins. In the recellularized vein, H&E-staining showed the presence of cells on the luminal surface of the vein.

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NATIVE HUMAN PROLACTIN, P Rabbit Anti-Human Androge succinate-CoA ligase, GDP Human PAI-1 (stable mutan RFP Expressing Human Saph Human, Adiponectin (Trime Native Human Lactoferrin, NATIVE HUMAN PROLACTIN, P Glycosylated Human PAI-1 Isopeptidase T (long form Rabbit Anti-Human Androge Growth Differentiation Fa

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[An improved method for stem cell derivation from human great saphenous vein].

The objectiue was to explore how to improve stem cell derivation from human great saphenous vein. After the saphenous vein was cut into small pieces, the cells of the vessel wall were obtained by tissue adherent method and digestion with type Ⅱ collagenase. The morphological changes of blood vessel wall were observed under inverted microscope. The survival of vascular wall cells was assessed by trypan blue staining. Stem cells doubly positive for CD34 and CD117 were sorted out by immunofluorescent staining and flow cytometry. The cells obtained by tissue adherence method exhibited signs of fibrotic changes and aging at the third passage (P3), while the cells extracted by enzymatic digestion still showed colony-like growth. Survival rates of these two groups of cells were (91.7±1.2)% and (97.2±0.7)%, (P=0.005). The results of flow cytometry showed that the positive rates of CD34 and CD117 double positive cells in these two groups were (0.16± 0.05)% and (0.44±0.07)%, respectively, with statistical significance (P=0.005). Immunofluorescent staining showed that the positive rates of double positive stem cells in the two groups were (89.41±2.06)% and (94.03±1.83)%, P<0.05 one week after the sorted stem cells were cultured. The positive rates of CD31, VEGF2 and SMA in the stem cells determined by flow cytometry were (0.12±0.01)%, (0.19±0.02)% and (0.45±0.01)%, respectively, which were not statistically different from those of the control groups. This could rule out substantial inclusion of mature endothelial cells and smooth muscle cells. Tube forming experiment confirmed that these vascular stem cells had developmental plasticity. More viable and morphologically healthy vascular stem cells can be derived by enzymatic digestion. These cells can be widely used in clinical and basic research.

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Assessment of a topical product based on polysulfated galactosaminoglycan as an adjuvant in the treatment of acute STP and stasis dermo-hypodermitis.

Superficial thrombophlebitis (STP) is a relatively frequent pathology characterized by possible extension to the deep venous circulation, with notable local inflammatory reaction which is treated by subcutaneous administration of Fondaparinux. Stasis dermo-hypodermitis is characterized by cutaneous hyperpigmentation and eczema, treatment for which consists of the use of drugs targeting endothelial cells (mesoglycan, FFPM, sulodexide). In this study we evaluated the impact of local application of a mixture of semi-synthetic polysulfated galactosaminoglycans on the regression rate of STP and dermo-hypodermitis in patients treated with best medical therapy (BMT).

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The effect of storage solutions, gene therapy, and antiproliferative agents on endothelial function and saphenous vein graft patency.

Vein graft failure remains a major concern after coronary artery bypass graft operations, and is initiated by loss of endothelial cell integrity. Preservation of saphenous vein grafts in the optimal solution after meticulous harvesting can limit the endothelial damage. Despite both experimental and clinical results in favor of buffered solutions, normal saline is still the most widely used solution. This review examines the literature to identify the most optimal storage solutions currently available for vein graft preservation.

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RFP Expressing Human Saph GFP Expressing Human Saph Human Saphenous Vein Endo Androgen Receptor , Mouse (5α,16β)-N-Acetyl-16-ac Androst-4-ene-3,17-dion-1 AZD-3514 Mechanisms: Andr Goat Anti-Human Androgen Androstadienone C19H26O C Androgen Receptor (Phosph Androstane-3a, 17b-diol 5 ∆1-Androstene-3β,17β-

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Effects Of Endothelin-1 On Intracellular Tetrahydrobiopterin Levels In Vascular Tissue.

Tetrahydrobiopterin (BH4) is the essential cofactor of endothelial nitric oxide synthase (eNOS) and intracellular levels of BH4 is regulated by oxidative stress. The aim of this paper was to describe the influence of exogenous endothelin-1 on intracellular BH4 and its oxidation products dihydrobiopterin (BH2) and biopterin (B) in a wide range of vascular tissue.

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MicroRNA-155 promotes neointimal hyperplasia through smooth muscle-like cell-derived RANTES in arteriovenous fistulas.

Arteriovenous fistula (AVF) suffers from a high number of failures caused by insufficient outward remodeling and venous neointimal hyperplasia formation. The aim was to investigate the exact mechanism by which microRNA-155 (miR-155) in the outflow vein of AVF is regulated.

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Kidney clear cell carcino Human Stromal Cell-Derive Actin, Smooth Muscle Ab-1 Cultrex In Vitro Angiogen Prostate cancer, PIN (pro Rabbit Anti-Cell death in Rabbit Anti-Cell death in Jurkat Cell Extract (Indu Kidney clear cell carcino Stat3 Peptide Inhibitor, Non small cell lung carci Biocidal ZF, spray disinf

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Diabetes Mellitus Induces Hyperreactivity of 5-Hydroxytryptamine (5-HT)-Induced Constriction in Human Internal Thoracic Artery and Is Associated with Increase in the Membrane Protein Level of 5-HT Receptor.

Studies indicate that 5-hydroxytryptamine (5-HT) released from activated platelets in coronary artery bypass grafting (CABG) induces 5-HT receptor-mediated graft spasm. We previously reported that 5-HT-induced constriction of human endothelium-denuded saphenous vein (SV) was significantly augmented in patients with diabetes mellitus (DM) than in patients without DM (non-DM), without changes in the levels of the membrane-bound 5-HT receptor of their smooth muscle cells. Although the internal thoracic artery (ITA) is the key graft conduit for CABG, the effect of DM on the ITA graft spasm is still unclear. Therefore, in this study, we investigated the effect of DM on 5-HT-induced vasoconstriction and the level of membrane-bound 5-HT receptor in ITA grafts. 5-HT-induced constriction of the isolated human endothelial-denuded ITA was significantly higher in patients with DM than in patients without DM. In addition, the level of the 5-HT receptor in the membrane fraction of human ITA smooth muscle cells was significantly higher in patients with DM than in those without DM. These results demonstrate that DM is a risk factor for CABG in both venous and arterial conduits, and that it differentially affects the level of the membrane-bound 5-HT receptor in the venous and arterial smooth muscle cells.

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Goat Anti-Human Serotonin Goat Anti-Human, Rat Sero Goat Anti-Human Prion Pro Goat Anti-Human MBD2 (iso Goat Anti-Human Glutathio Rabbit Anti-TNIP2 ABIN2 T Human Internal Mammary Ar Rabbit Anti-Cell death in Goat Anti-Human NHERF2 (i Goat Anti-Human Ribosomal Anti AGO2 Human, Monoclon Rabbit Anti-APIP Apaf1 In

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Upregulation of miR-126-3p promotes human saphenous vein endothelial cell proliferation and prevents vein graft neointimal formation and .

Poor long-term patency of vein grafts remains an obstacle in coronary artery bypass grafting (CABG) surgery using an autologous saphenous vein graft. Recent studies have revealed that miR-126-3p promotes vascular integrity and angiogenesis. We aimed to identify the role of miR-126-3p in the setting of vein graft disease and investigate the value of miR-126-3p agomir as a future gene therapy in vein graft failure. Expression analysis of circulating miR-126-3p in plasma from CABG patients established the basic clues that miR-126-3p participates in CABG. The results indicated that elevated miR-126-3p expression significantly improved proliferation and migration in human saphenous vein endothelial cells (HSVECs) by targeting sprouty-related protein-1 (SPRED-1) and phosphatidylinositol-3-kinase regulatory subunit 2 (PIK3R2), but not in human saphenous vein smooth muscle cells (HSVSMCs). Moreover, the therapeutic potential of miR-126-3p agomir was demonstrated in cultured human saphenous vein (HSV) . Finally, local delivery of miR-126-3p agomir was confirmed to enhance reendothelialization and attenuate neointimal formation in a rat vein arterialization model. In conclusion, we provide evidence that upregulation of miR-126-3p by agomir possesses potential clinical value in the prevention and treatment of autologous vein graft restenosis in CABG.

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RFP Expressing Human Saph GFP Expressing Human Saph Human Saphenous Vein Endo RFP Expressing Human Umbi GFP Expressing Human Umbi Mouse Anti-Human Endothel Plasma Membrane GFP Tag H Human Umbilical Vein Endo Mitochondria GFP Tag Huma Human Bladder Microvascul Human Dermal Lymphatic Mi Human Coronary Artery End

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