Study on the Mechanism of Fibronectin Adhesion to NIH3T3 cell Stimulated by Retinoic Acid

Jian-Yu He1, Li-Huan Cao, Yue-Bin Li

  • 1Department of Biochemistry, Shanghai Medical University, Ministry of Public Health Key laboratory of glycoconjugates Research, Shanghai 200032, China.

Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao Acta Biochimica Et Biophysica Sinica
|August 14, 2002
PubMed

Insights

Retinoic acid (RA) enhances NIH3T3 cell adhesion to fibronectin by altering cell surface glycoproteins. This suggests RA

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Retinoic acid (RA) is known to induce cell differentiation and cause physiological alterations.
  • Its role in cell adhesion to the extracellular matrix, specifically fibronectin (Fn), is not well understood.
  • RA may revert tumor cells to normal cell phenotypes.

Purpose of the Study:

  • To investigate the effect of retinoic acid (RA) on the adhesion of NIH3T3 cells to fibronectin (Fn).
  • To elucidate the molecular mechanisms underlying RA-mediated changes in cell adhesion.

Main Methods:

  • NIH3T3 cells were treated with varying concentrations of RA.
  • Cell adhesion to Fn and poly-L-lysine was measured.
  • Integrin alpha(5) and beta(1) subunit expression was analyzed using flow cytometry (FCM).
  • Incorporation of (3)H-mannose and oligosaccharide composition were analyzed.

Main Results:

  • RA significantly increased NIH3T3 cell adhesion to Fn in a dose-dependent manner (20% increase at 32 µmol/L RA).
  • No significant change was observed in cell adhesion to poly-L-lysine.
  • RA treatment did not alter the cell surface expression of integrin alpha(5) and beta(1) subunits.
  • RA increased (3)H-mannose incorporation by 53% and altered oligosaccharide types, including tri- or tetra-antennary and bisecting complex types.

Conclusions:

  • Retinoic acid enhances NIH3T3 cell adhesion to fibronectin.
  • The mechanism involves alterations in the amount and type of cell surface glycoprotein oligosaccharides, not changes in integrin expression.
  • These findings provide new insights into the role of RA in regulating cell-matrix interactions.

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