Toxicarioside A, isolated from tropical Antiaris toxicaria, blocks endoglin/TGF-beta signaling in a bone marrow stromal cell line

文献类型： 外文期刊

第一作者： Li, Yue-Nan

作者： Li, Yue-Nan;Huang, Feng-Ying;Mei, Wen-Li;Dai, Hao-Fu;Zhou, Peng;Li, Yue-Nan;Huang, Feng-Ying;Mei, Wen-Li;Dai, Hao-Fu;Zhou, Peng;Li, Yue-Nan;Huang, Feng-Ying;Guo, Jun-Li;Tan, Guang-Hong

作者机构：

关键词： Toxicarioside A;Endoglin;Transforming growth factor-beta;Signal pathway;Cell proliferation

期刊名称：ASIAN PACIFIC JOURNAL OF TROPICAL MEDICINE （ 影响因子：1.226； 五年影响因子：2.285 ）

ISSN： 1995-7645

年卷期： 2012 年 5 卷 2 期

页码：

收录情况： SCI

摘要： Objective: To investigate possible mechanism of toxicarioside A in HS-5 bone stromal cells. Methods: HS-5 bone stromal cells were cultured in media supplemented with various concentrations of toxicarioside A or control Dmso (not treatment). Endoglin and TGF were detected by Northern and Western blot analysis and quantified in a standard method. Downstream molecules of endoglin and TGF-beta (Smad1, Smad2 and their active phosphorlated counterparts, pSmad1 and pSmad2) were also detected and quantified by Western blot analysis. In addition, cell proliferation assay and small interfering RNA (siRNA) against endoglin were used to certificate the function of endolgin in the HS-5 cells. Results: Compared with the not treated (0 mu g/mL) or HMSO treated control HS-5 cells, HS-5 cells treated with toxicarioside A were found significant attenuation of endolgin and TGF p expression. Significant inhibition of cell proliferation was also found in the HS-5 cells treated with toxicarioside A. ALK1-related Smadl and ALK5-related Srnad2 were decreased in HS-5 cells treated with toxicarioside A. In addition, phosphorylated Smadl (pSmad1) and Smad2 (pSmad2) were also found attenuation in toxicarioside A treated HS-5 cells. RNA interference showed that blockage of endoglin by siRNA also decreased Smadl and Smad2 expression in HS-5 cells. Conclusions: Our results indicate that tosicatioside A can influence bone marrow stromal HS-5's function and inhibit HS-5 cell proliferation by alteration of endoglin-related ALK1 (Smadl) and ALIO (Smad2) signaling.

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