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Updated: Sep 30, 2026

Examining the Dynamics of Cellular Adhesion and Spreading of Epithelial Cells on Fibronectin During Oxidative Stress
Published on: October 13, 2019
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.
Abstract:
Retinoic acid (RA) is an inducer of cell differentiation. Recently, it was discovered that RA widely works on cells, causing a series of physiological alterations, and may make the tumor cell differentiation back to the normal cells, but little is known about its role in the adhesion of the cell to the extracellular matrix (Fn). We observed that RA increased the ability of NIH3T3 cells to adhere to Fn in a dose-dependent manner. The cell adhesion to fibronectin was promoted by 20% with 32 &mgr;mol/L RA, but not to polylysine. We use anti-integrin alpha(5)-subunit and beta(1)-subunit monoclonal antibodies to measure the amounts of integrin on the cell surface by FCM. It showed that the amounts of alpha(5) and beta(1) subunits of integrin did not change when the NIH3T3 cells were treated with RA for 24 h. But the incorporation of (3)H-mannose was increased by 53 % and those of tri- or tetra- antennary or bisecting complex type oligosaccharides were increased by 13 %. These results indicated that the increased adhesion of the cells to Fn in presence of RA may be caused by altering amounts and types of the oligosaccharides of the glycoprotein on the cell surface.
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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