Imbalance in matrix metalloproteinases and tissue inhibitor of metalloproteinases from splenic veins and great saphenous veins under high hemodynamics

Abstract

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.