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Transforming growth factor beta 1 impairs benign prostatic luminal epithelial cell monolayer barrier function
Feng Li1,2,3, Laura E Pascal3, Ke Wang1,3
1Department of Urology, The First Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
American Journal of Clinical and Experimental Urology
|March 27, 2020
Summary
Transforming growth factor beta 1 (TGF-β1) increases benign prostatic hyperplasia (BPH) epithelial barrier permeability by reducing claudin 1 expression and inhibiting tight junction formation. This suggests TGF-β1 plays a key role in BPH development.
Area of Science:
- Urology
- Cell Biology
- Molecular Biology
Background:
- Benign prostatic hyperplasia (BPH) is associated with increased epithelial barrier permeability.
- Transforming growth factor beta 1 (TGF-β1) is upregulated in BPH and affects E-cadherin expression.
- The precise mechanism by which TGF-β1 influences BPH epithelial barrier function remains unclear.
Purpose of the Study:
- To investigate the impact of TGF-β1 on the epithelial barrier and tight junctions in benign prostatic epithelial cells.
- To determine the effect of TGF-β1 on the expression of E-cadherin and claudin 1.
- To assess the role of TGF-β1 in BPH pathogenesis by examining its effect on prostate epithelial permeability.
Main Methods:
- In vitro studies using benign prostatic epithelial cell lines (BHPrE1, BPH-1) treated with TGF-β1.
- Transepithelial electrical resistance (TEER) measurements and FITC-dextran diffusion assays to assess barrier permeability.
- Quantitative PCR (qPCR) and transmission electron microscopy (TEM) to evaluate tight junction proteins (E-cadherin, claudin 1).
- Laser capture micro-dissection (LCM) combined with qPCR to analyze gene expression in patient tissues.
Main Results:
- TGF-β1 treatment significantly decreased TEER and increased FITC-dextran diffusion in cell monolayers, indicating increased permeability.
- TGF-β1 reduced the mRNA expression of the tight junction protein claudin 1 in cultured cells.
- Claudin 1 mRNA was downregulated in the luminal epithelial cells of BPH nodules compared to normal prostate tissue, while E-cadherin mRNA was not significantly affected.
Conclusions:
- TGF-β1 increases the permeability of the benign prostatic epithelial barrier by downregulating claudin 1 expression and inhibiting tight junction formation.
- The findings suggest that TGF-β1 plays a significant role in the pathogenesis of BPH by compromising the epithelial barrier integrity.
- Targeting TGF-β1 signaling may offer a therapeutic strategy for managing BPH.
