Department of Vascular Surgery and Transplantology, Medical University of Bialystok, PL-15-276 Bialystok, Poland.
Pathobiology. 2010;77(1):1-6. doi: 10.1159/000272948. Epub 2010 Feb 25.
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.
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.
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.
静脉壁细胞外基质的重塑与静脉曲张的发病机制有关，其中转化生长因子β（TGF-β）可能发挥作用。本研究旨在评估静脉曲张组织中 TGF-β信号通路及其受体（TGF-βRII）和磷酸化受体调节 Smads（p-Smad2/3）的表达。
研究材料为静脉曲张患者手术切除的曲张静脉，对照材料为行下肢动脉旁路术的患者正常大隐静脉。采用 RT-PCR 检测 TGF-βRII mRNA 的表达，Western blot 检测 TGF-βRII 和 p-Smad2/3 蛋白的表达。
与正常静脉（100±26%）相比，曲张静脉中 TGF-βRII mRNA 水平明显升高（287±24%）。受体蛋白表达反映了 mRNA 水平的变化，曲张静脉中 TGF-βRII 蛋白表达明显升高（290±21%），与对照组（100±16%）相比差异有统计学意义。与正常静脉（100±9%）相比，曲张静脉中 TGF-βRII 表达增强伴随着 p-Smad2/3 蛋白表达的增加（257±19%）。
曲张静脉壁中 TGF-βRII 的表达和激活增加可能与 TGF-β（1）相关的细胞外基质重塑有关，并支持其在疾病发病机制中的作用。
