Human trophoblast requires galectin-3 for cell migration and invasion

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Abstract

Invasive extravillous cytotrophoblast of the human placenta expresses galectins-1, -3, and -8 in vivo and in vitro. This study aimed to investigate the potential role of galectin-3 in cell migration and invasion, using recombinant human galectin-3 (rhgalectin-3), small molecule galectin inhibitor I 47 , and galectin-3 silencing. HTR-8/SVneo cell migration was stimulated by rhgalectin-3 and reduced by I 47 , which could be neutralised by rhgalectin-3. Inhibitor specificity and selectivity for the galectins expressed in extravillous trophoblast were validated in solid phase assays using recombinant galectin-1, -3, -8, confirming selectivity for galectin-3. HTR-8/SVneo cell migration and invasion, and invasion by isolated trophoblast cells in primary culture were significantly reduced in the presence of I 47, which could be restored by rhgalectin-3. Upon HTR-8/SVneo cell treatment with galectin-3 siRNA both LGALS3 and galectin-3 protein were dramatically decreased. Silencing of galectin-3 induced significant reduction in cell migration and invasion, which was restored by rhgalectin-3. The influence on known mediators of cell invasion, MMP2 and -9, and integrins α 1 , α 5 , and β 1 was followed in silenced cells, showing lower levels of MMPs and a large reduction in integrin subunit β 1 . These results show that galectin-3 acts as a pro-invasive autocrine/paracrine factor in trophoblast in vitro.

Detaljer

Författare
  • Bojić-Trbojević
  • M. Jovanović Krivokuća
  • A. Vilotić
  • N. Kolundžić
  • I. Stefanoska
  • F. Zetterberg
  • U. J. Nilsson
  • H. Leffler
  • Lj Vićovac
Enheter & grupper
Externa organisationer
  • University of Belgrade
  • King's College London
  • Galecto Biotech AB
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Cell- och molekylärbiologi
Originalspråkengelska
Artikelnummer2136
TidskriftScientific Reports
Volym9
Utgivningsnummer1
StatusPublished - 2019 feb 14
PublikationskategoriForskning
Peer review utfördJa