lps tlr4 signaling enhances tgf response through downregulating bambi during prostatic hyperplasia

www.nature.com/scientificreports OPEN received: 05 February 2016 accepted: 12 May 2016 Published: 31 May 2016 LPS/TLR4 Signaling Enhances TGF-β Response Through Downregulating BAMBI During Prostatic Hyperplasia Yao He1, Zhenyu Ou1, Xiang Chen1, Xiongbing Zu1, Longfei Liu1, Yuan Li1, Zhenzhen Cao2, Minfeng Chen1, Zhi Chen1, Hequn Chen1, Lin Qi1 & Long Wang1 Compelling evidence suggests that benign prostatic hyperplasia (BPH) development involves accumulation of mesenchymal-like cells derived from the prostatic epithelium by epithelialmesenchymal transition (EMT) Transforming growth factor (TGF)-β induces EMT phenotypes with low E-cadherin and high vimentin expression in prostatic epithelial cells Here we report that LPS/TLR4 signalling induces down-regulation of the bone morphogenic protein and activin membrane-bound inhibitor (BAMBI), which enhances TGF-β signalling in the EMT process during prostatic hyperplasia Additionally, we found that the mean TLR4 staining score was significantly higher in BPH tissues with inflammation compared with BPH tissues without inflammation (5.13 ± 1.21 and 2.96 ± 0.73, respectively; P