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Alleviation of TGF-β1 induced tubular epithelial-mesenchymal transition via the δ-opioid receptor

Fengbao Luo1, Renfang Xu1, Guanglai Song1

  • 1Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, China.

The FEBS Journal
|June 21, 2020
PubMed

Insights

The δ-opioid receptor (DOR) inhibits renal fibrosis in kidney cells by blocking transforming growth factor-β1 (TGF-β1) induced changes. DOR activation protects against kidney disease progression by targeting key fibrotic signaling pathways.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pharmacology

Background:

  • Renal fibrosis is a hallmark of chronic kidney disease (CKD) progression.
  • Transforming growth factor-β1 (TGF-β1) is a key mediator in the development of renal fibrosis.
  • Understanding the molecular mechanisms underlying renal fibrosis is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the role of the δ-opioid receptor (DOR) in TGF-β1-induced renal fibrosis in rat renal proximal tubular epithelial cells (NRK-52E).
  • To elucidate the underlying molecular mechanisms and signaling pathways involved in DOR's effect on renal fibrosis.
  • To evaluate the potential of DOR as a therapeutic target for mitigating renal fibrosis.

Main Methods:

  • NRK-52E cells were treated with TGF-β1, a DOR agonist (UFP-512), or a DOR antagonist (naltrindole).
  • Cell viability, morphology, and migration were assessed.
  • Western blotting was used to analyze the expression of extracellular matrix proteins (Fibronectin), epithelial-mesenchymal transition (EMT) markers (E-cadherin, α-SMA), signaling molecules (p-Smad3, p-Akt, p-p38), and EMT regulators (Snail).

Main Results:

  • TGF-β1 induced fibrotic changes, including increased Fibronectin, α-SMA, p-Smad3, Snail, p-Akt, and p-p38, and decreased E-cadherin.
  • TGF-β1 also promoted cell migration and altered cell morphology.
  • DOR activation by UFP-512 effectively counteracted TGF-β1-induced fibrotic changes, blocked cell migration, and normalized marker expression, including p-Smad3, p-Akt, and p-p38.

Conclusions:

  • The δ-opioid receptor (DOR) plays a protective role against renal fibrosis in proximal tubular epithelial cells.
  • DOR activation inhibits TGF-β1-induced renal fibrosis by modulating the TGF-β/Smad, Akt, and p38 MAPK signaling pathways.
  • DOR represents a potential therapeutic target for treating renal fibrosis and chronic kidney disease.
Keywords:
DOREMTTGF-β1renal fibrosissignaling pathway

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