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Objective: The contribution of hypoxia to the pathophysiology of vascular smooth muscle cells (VSMCs) has not yet been fully elucidated. This study evaluated the effect of hypoxia on the phenotype and function of SMCs derived from the human normal great saphenous veins (NGSVs). Methods: Fifteen NGSV tissue samples were collected. SMCs were isolated and cultured. Proliferation, migration, adhesion, senescence, and the structure of cytoskeletal filaments in SMCs were observed. mRNA and protein expression of Bax, Bcl-2, caspase-3, matrix metalloproteinases (MMP)-2, MMP-9, tissue inhibitor of metalloproteinases (TIMP)-1, and TIMP-2 was detected by fluorescent quantitative polymerase chain reaction and immunoblotting in the cobalt chloride (CoCl2) and the control groups. Results: A decrease in the number of cytoskeletal filaments was observed. mRNA and protein expression of Bas and caspase-3 was significantly decreased, while the quantity of proliferation, migration, adhesion, senescence, and mRNA and protein expression of Bcl-2, MMP-2, MMP-9, TIMP-1, and TIMP-2 in SMCs in the CoCl2 group were significantly increased compared with the control group. Conclusion: Under hypoxic conditions, the phenotype and function of SMCs derived from the human NGSVs were dysregulated, suggesting that VSMCs switch from the contractile phenotype to the secretory or synthetic phenotype, and more dedifferentiate, resulting in extracellular matrix deposition and apoptotic decrease through the intrinsic pathway. [ABSTRACT FROM AUTHOR]

Objectives: Superficial venous thrombosis (SVT) is the complications of varicose great saphenous veins (VGSVs), but its pathogenesis remains unclear. This study was designed to measure the changes in expression of matrix metalloproteinases (MMPs) and the tissue inhibitor of metalloproteinases (TIMPs) from SVT, VGSVs, and great saphenous veins (GSVs). Methods: In the venous walls of the three groups, the expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 proteins, protein-positive expression ratios, mRNA expression, and protein expression were determined by immunohistochemistry, polymerase chain reaction, and western blot. Results: The MMP-2, MMP-9, TIMP-1, and TIMP-2 protein-positive expression ratios, mRNA and protein expression in the SVT group were significantly higher than those in the VGSV and the GSV groups. The corresponding expression in the VGSV group were significantly higher than those in the GSV group. Conclusion: Disequilibrium of MMPs and TIMPs in SVT wall occurs due to underlying high hydrostatic pressure and inflammation. These results suggested that MMPs and TIMPs participate in the process of venous wall remodeling. [ABSTRACT FROM AUTHOR]

Objectives: Varicose vein is a common disorder involving extensive venous dilation and remodeling, yet the underlying mechanism is unclear. Studies have shown increased expression of matrix metalloproteinases in human varicose veins and animal models of venous hypertension. We investigated the differences in matrix metalloproteinases and tissue inhibitor of metalloproteinases from human splenic veins and great saphenous veins under high hemodynamics. Methods: Seventy-two human diseased splenic vein, splenic vein, varicose great saphenous vein, and great saphenous vein specimens were collected. The mRNA and protein expression of matrix metalloproteinase-2, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and tissue inhibitor of metalloproteinase-2 were determined. Results: The mRNA expression and protein positive expression ratio of matrix metalloproteinase-2, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and tissue inhibitor of metalloproteinase-2 as well as the content of relative-protein expression were significantly increased in the diseased splenic veins and varicose great saphenous veins compared with the splenic veins and great saphenous veins (P < 0.05). The varicose great saphenous vein-to-great saphenous vein ratio in the protein positive expression ratio and mRNA expression were significantly increased compared with the diseased splenic vein-to-saphenous vein ratio (P < 0.05). There was no significant change in the content of relative-protein expression of the varicose great saphenous vein-to-great saphenous vein and diseased splenic vein-to-splenic vein ratios analyzed by Western blot (P >0.05). Conclusion: Under high hemodynamics, dysequilibrium of matrix metalloproteinases and tissue inhibitor of metalloproteinases from human splenic veins and great saphenous veins may be one of the molecular mechanisms underlying vascular remodeling. [ABSTRACT FROM AUTHOR]