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Sources of Funding: This study was supported by Grant No. 31170907, No. 31370951, No. 81470927 and No.81300579 from the National Natural Science Foundation of China, Grant No. 2014SCU04B21 from Fund for Distinguished Young Scholars of Sichuan University, Grant No.JH2014053 from Academic Leader Traning Fund of Sichuan Province and Grant No. JH2015017 from Application-oriented Foundation of Committee Organization Department of Sichuan Provincial Party. _x000D_

Introduction

Bladder Outlet Obstruction(BOO) is one of the pathological changes resulted from abnormal intravesical pressure. We investigated the effects of hydrostatic pressure and mechanic strain on the release of inflammatory cytokines in rat and human bladder smooth muscle cells (HBSMCs) and tried to explore the relationship of Il-6 and the remodeling of of extracellular matrix of human bladder smooth muscle cells.

Methods

Animal model of bladder outlet obstruction was induced by urethra ligation. HBSMCs were subjected to elevated hydrostatic pressure and mechanic strain. The expression of inflammatory genes were analysed using DNA microarrays. IL-6 was confirmed by quantitative RT–PCR and immunohistochemical staining. Specificity of the IL-6 was determined with qRT-PCR with small interfering ribonucleic acid transfection and iL-6 receptor inhibitor (SC144). And specificity of the  downstream was determined with qRT-PCR with small interfering ribonucleic acid transfection and STAT3 inhibitor(S31-201)._x000D_

Results

In BOO, inflammatory genes were remarkably induced. in vitro, the expressions of IL-6 were significantly increased. Hydrostatic pressure and mechanic strain both promoted the IL-6 mRNA expression. Additionally, IL-6 increased the mRNA expression of MMP7 and TIMP1, decreased the mRNA expression of collagen and fibronectin. The “knock- down” of activation of IL-6 receptor using target small interfering ribonucleic acid transfection and inhibitor iL-6 receptor(SC144) significantly decreased the expression of MMP7 ,TIMP1 and partially increased the collagen and fibronectin. Additionally, pressure-induced MMP7 andTIMP1 were partially suppressed by STAT3 pathway using target small interfering ribonucleic acid transfection and inhibitor STAT3 (S31-201).

Conclusions

IL-6 was involved in the remodeling of extracellular matrix in HBSMCs under mechanic strain and hydrostatic pressure, indicating that IL-6 play an important role under in BOO.

Funding

This study was supported by Grant No. 31170907, No. 31370951, No. 81470927 and No.81300579 from the National Natural Science Foundation of China, Grant No. 2014SCU04B21 from Fund for Distinguished Young Scholars of Sichuan University, Grant No.JH2014053 from Academic Leader Traning Fund of Sichuan Province and Grant No. JH2015017 from Application-oriented Foundation of Committee Organization Department of Sichuan Provincial Party. _x000D_