OBJECTIVE(S): Extracellular matrix remodeling in the vein wall is involved in varicose vein pathogenesis, with transforming growth factor beta(1) (TGF-beta(1)) playing a potential role. The aim of the study was to assess the TGF-beta signaling pathway including its receptor (TGF-beta RII) and phosphorylated receptor-regulated Smads (p-Smad2/3) in varicose veins. METHODS: Varicose veins from patients undergoing varicose vein surgery were the studied material, whereas normal greater saphenous veins from patients undergoing infrainguinal arterial bypass surgery were the control material. Expression of TGF-beta RII mRNA was assessed with RT-PCR, whereas expression of TGF-beta RII and p-Smad2/3 proteins was assessed with Western blot. RESULTS: A significantly increased TGF-beta RII mRNA level was found in varicose veins (287 +/- 24%), when compared with normal veins (100 +/- 26%). The receptor protein expression reflected a changed mRNA level with significantly increased TGF-beta RII protein in varicose veins (290 +/- 21%), when compared with controls (100 +/- 16%). Enhanced TGF-beta RII expression was accompanied by increased p-Smad2/3 protein expression in varicose veins (257 +/- 19%) in comparison with normal veins (100 +/- 9%). CONCLUSION(S): Increased TGF-beta RII expression and activation in the wall of varicose veins may be involved in extracellular matrix remodeling related to TGF-beta(1) and supports its role in the disease pathogenesis. Copyright 2010 S. Karger AG, Basel.
OBJECTIVE(S): Extracellular matrix remodeling in the vein wall is involved in varicose vein pathogenesis, with transforming growth factor beta(1) (TGF-beta(1)) playing a potential role. The aim of the study was to assess the TGF-beta signaling pathway including its receptor (TGF-beta RII) and phosphorylated receptor-regulated Smads (p-Smad2/3) in varicose veins. METHODS: Varicose veins from patients undergoing varicose vein surgery were the studied material, whereas normal greater saphenous veins from patients undergoing infrainguinal arterial bypass surgery were the control material. Expression of TGF-beta RII mRNA was assessed with RT-PCR, whereas expression of TGF-beta RII and p-Smad2/3 proteins was assessed with Western blot. RESULTS: A significantly increased TGF-beta RII mRNA level was found in varicose veins (287 +/- 24%), when compared with normal veins (100 +/- 26%). The receptor protein expression reflected a changed mRNA level with significantly increased TGF-beta RII protein in varicose veins (290 +/- 21%), when compared with controls (100 +/- 16%). Enhanced TGF-beta RII expression was accompanied by increased p-Smad2/3 protein expression in varicose veins (257 +/- 19%) in comparison with normal veins (100 +/- 9%). CONCLUSION(S): Increased TGF-beta RII expression and activation in the wall of varicose veins may be involved in extracellular matrix remodeling related to TGF-beta(1) and supports its role in the disease pathogenesis. Copyright 2010 S. Karger AG, Basel.