Galectin-1 suppresses α2(I) collagen through Smad3 in renal epithelial cells

K. Okano*, K. Uchida, K. Nitta, T. Hayashida

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Transforming growth factor (TGF-β1) promotes renal fibrogenesis through activation of Smads. Galectin-1 is reported to prevent experimental glomerulonephritis. Here we investigated the fact that transfected galectin-1 significantly suppressed the transcription of α2(I) collagen (COL1A2) in TGF-β1- activated human renal epithelial cells. Conversely, galectin-1 silencing RNA reduced secretion of type I collagen by HKC cells. Galectin-1 significantly decreased activation of a TGF-β1-responsive reporter construct and of a minimal reporter construct that contains four repeats of the Smad binding element (SBE). Galectin-1 had no effect on phosphorylation of Smad3 at the linker region and C-terminus, whereas it decreased affinity of Smad3 to the SBE. Additionally, the inhibitory effect of galectin-1 disappeared using a mutated reporter construct, 376 m-LUC, in which a potential Smad recognition site within the promoter is mutated. Taken together, the results suggest that galectin-1 decreases Smad3-complex from binding to the SBE, down-regulating transcription of COL1A2 in TGF-β1-stimulated renal epithelial cells.

Original languageEnglish (US)
Pages (from-to)3304-3311
Number of pages8
JournalCellular and Molecular Life Sciences
Volume65
Issue number20
DOIs
StatePublished - Oct 2008
Externally publishedYes

Funding

Keywords

  • Galectin-1
  • Renal fibrosis
  • SBE
  • Smad3
  • TGF-β1
  • Type I collagen

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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