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Identification and Analysis of Differentially Expressed Genes in Human Saphenous Vein Endothelial Cells Overexpressing Domain-Containing mTOR-Interacting Protein (DEPTOR) by RNA-Seq.

BACKGROUND Autologous saphenous vein is the most common choice for coronary artery bypass grafting. This study was conducted to identify and characterize differentially expressed genes (DEGs) induced by overexpressing DEPTOR in human saphenous vein endothelial cells (hsVECs) that might play roles in restenosis. MATERIAL AND METHODS hsVECs isolated from the saphenous veins were transfected with DEPTOR overexpression vector and analyzed for mTOR expression. RNA was prepared from the cells and sequenced using high-throughput sequencing technology (RNA-Seq). The DEGs were analyzed based on enrichment scores in GO terms and KEGG pathways. RESULTS The cells had typical hsVEC morphology and characteristics based on the HE staining and immunohistochemical and immunofluorescence assays. The expression of mTOR increased, and 102 genes were upregulated, and 409 genes were downregulated after DEPTOR overexpression. KEGG analysis showed that the DEGs were mainly enriched in 20 signal pathways, such as Focal adhesion and ECM-receptor interaction pathways. The DEGs were enriched in GO terms such as integrin binding and glycosaminoglycan binding. For cellular components, GO analysis revealed that the DEGs were enriched in main axon, plasma membrane part, cell junction, and proteinaceous extracellular matrix. DEGs included many cytokines, such as bone morphogenetic protein-7, interleukin-8, interleukin-1ß, and inhibin, which have important effects on vascular growth and inflammation. CONCLUSIONS The overexpression of DEPTOR in hsVECs results in DEGs that are involved in cell proliferation and differentiation, intercellular junction, and extracellular matrix receptor. These findings may provide valuable molecular information for improving venous permeability through manipulation of DEPTOR and related mTOR pathways.

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Normal Saline solutions cause endothelial dysfunction through loss of membrane integrity, ATP release, and inflammatory responses mediated by P2X7R/p38 MAPK/MK2 signaling pathways.

Resuscitation with 0.9% Normal Saline (NS), a non-buffered acidic solution, leads to increased morbidity and mortality in the critically ill. The goal of this study was to determine the molecular mechanisms of endothelial injury after exposure to NS. The hypothesis of this investigation is that exposure of endothelium to NS would lead to loss of cell membrane integrity, resulting in release of ATP, activation of the purinergic receptor (P2X7R), and subsequent activation of stress activated signaling pathways and inflammation. Human saphenous vein endothelial cells (HSVEC) incubated in NS, but not buffered electrolyte solution (Plasma-Lyte, PL), exhibited abnormal morphology and increased release of lactate dehydrogenase (LDH), adenosine triphosphate (ATP), and decreased transendothelial resistance (TEER), suggesting loss of membrane integrity. Incubation of intact rat aorta (RA) or human saphenous vein in NS but not PL led to impaired endothelial-dependent relaxation which was ameliorated by apyrase (hydrolyzes ATP) or SB203580 (p38 MAPK inhibitor). Exposure of HSVEC to NS but not PL led to activation of p38 MAPK and its downstream substrate, MAPKAP kinase 2 (MK2). Treatment of HSVEC with exogenous ATP led to interleukin 1β (IL-1β) release and increased vascular cell adhesion molecule (VCAM) expression. Treatment of RA with IL-1β led to impaired endothelial relaxation. IL-1β treatment of HSVEC led to increases in p38 MAPK and MK2 phosphorylation, and increased levels of arginase II. Incubation of porcine saphenous vein (PSV) in PL with pH adjusted to 6.0 or less also led to impaired endothelial function, suggesting that the acidic nature of NS is what contributes to endothelial dysfunction. Volume overload resuscitation in a porcine model after hemorrhage with NS, but not PL, led to acidosis and impaired endothelial function. These data suggest that endothelial dysfunction caused by exposure to acidic, non-buffered NS is associated with loss of membrane integrity, release of ATP, and is modulated by P2X7R-mediated inflammatory responses.

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Plasma Membrane GFP Tag H GPCR Signaling to MAPK ER H+ATPase | plasma membran Tris Buffered Saline + T Human Tonsil Microvascula Blastoma tissue array wit IpPore track etched membr p38â„¢ GFP Uterine cervix cancer tis Ovarian cancer and normal ATP6B Inflammation (Mouse) Anti

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Hydrogen sulfide-releasing peptide hydrogel limits the development of intimal hyperplasia in human vein segments.

Currently available interventions for vascular occlusive diseases suffer from high failure rates due to re-occlusive vascular wall adaptations, a process called intimal hyperplasia (IH). Naturally occurring hydrogen sulfide (HS) works as a vasculoprotective gasotransmitter in vivo. However, given its reactive and hazardous nature, HS is difficult to administer systemically. Here, we developed a hydrogel capable of localized slow release of precise amounts of HS and tested its benefits on IH. The HS-releasing hydrogel was prepared from a short peptide attached to an S-aroylthiooxime HS donor. Upon dissolution in aqueous buffer, the peptide self-assembled into nanofibers, which formed a gel in the presence of calcium. This new hydrogel delivered HS over the course of several hours, in contrast with fast-releasing NaHS. The HS-releasing peptide/gel inhibited proliferation and migration of primary human vascular smooth muscle cells (VSMCs), while promoting proliferation and migration of human umbilical endothelial cells (ECs). Both NaHS and the HS-releasing gel limited IH in human great saphenous vein segments obtained from vascular patients undergoing bypass surgery, with the HS-releasing gel showing efficacy at a 5x lower dose than NaHS. These results suggest local perivascular HS release as a new strategy to limit VSMC proliferation and IH while promoting EC proliferation, hence re-endothelialization. STATEMENT OF SIGNIFICANCE: Arterial occlusive disease is the leading cause of death in Western countries, yet current therapies suffer from high failure rates due to intimal hyperplasia (IH), a thickening of the vascular wall leading to secondary vessel occlusion. Hydrogen sulfide (HS) is a gasotransmitter with vasculoprotective properties. Here we designed and synthesized a peptide-based HS-releasing hydrogel and found that local application of the gel reduced IH in human vein segments obtained from patients undergoing bypass surgery. This work provides the first evidence of HS efficacy against IH in human tissue, and the results show that the gel is more effective than NaHS, a common instantaneous HS donor.

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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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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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Alpha Smooth Muscle Actin Monoclonal Anti-Actin, β Monoclonal Anti Actin, β Anti bodywall muscle cell Plasma Membrane GFP Tag H Human Saphenous Vein Endo Monoclonal Anti Actin, β Anti-bodywall muscle cell Actin, Alpha-Smooth Musc Human Umbilical Vein Endo Rabbit Anti-Bovine Smooth Sarcoma tissue array of s

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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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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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