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E-cadherin is downregulated in benign prostatic hyperplasia and required for tight junction formation and permeability barrier in the prostatic epithelial cell monolayer.

Feng LiLaura E PascalDonna B StolzKe WangYibin ZhouWei ChenYadong XuYule ChenRajiv DhirAnil V ParwaniJoel B NelsonDonald B DeFrancoNaoki YoshimuraGoundappa K BalasubramaniJeffrey R GingrichJodi K MaranchieBruce L JacobsBenjamin J DaviesRonald L HrebinkoJoel D BigleyDawn McBridePeng GuoDalin HeZhou Wang
Published in: The Prostate (2019)
Our results indicate that tight junctions are compromised in BPH and loss of E-cadherin is potentially an important underlying mechanism, suggesting targeting E-cadherin loss could be a potential approach to prevent or treat BPH.
Keyphrases
  • benign prostatic hyperplasia
  • lower urinary tract symptoms
  • blood brain barrier
  • single molecule
  • endothelial cells
  • prostate cancer
  • human health
  • drug delivery
  • risk assessment
  • climate change