Basic fibroblast growth factor is essential to maintain endothelial progenitor cell phenotype in TR-BME2 cells

Area of Science:

• Cell Biology
• Vascular Biology
• Stem Cell Research

Background:

• Endothelial progenitor cells (EPCs) possess the potential to differentiate into endothelial cells and smooth muscle cells (SMCs).
• Previous research indicated that TR-BME2 cells, a model for EPCs, exhibited SMC-like characteristics when cultured in media lacking endothelial cell growth factors (ECGF).

Purpose of the Study:

• To investigate the specific role of basic fibroblast growth factor (bFGF), an ECGF, in regulating EPC differentiation.
• To elucidate the mechanisms by which bFGF influences EPC phenotype and function.

Main Methods:

• Confirmation of basic fibroblast growth factor receptor (FGFR-1) mRNA expression in TR-BME2 cells under varying ECGF conditions.
• Assessment of TR-BME2 cell differentiation into SMCs in ECGF-deprived versus ECGF-rich media, with and without bFGF.
• Analysis of marker expression for undifferentiated EPCs (CD133) and SMCs (smooth muscle α-actin (SMA), smooth muscle protein 22 (SM22)).
• Evaluation of TR-BME2 cell proliferation and tube formation capacity in response to bFGF and vascular endothelial cell growth factor (VEGF).

Main Results:

• ECGF deprivation induced TR-BME2 cell differentiation into contractile SMCs, reduced CD133 expression and proliferation, and increased SMA and SM22 mRNA levels.
• The presence of bFGF diminished the effects of ECGF deprivation, suppressing SMC differentiation markers and preserving CD133 expression and proliferation.
• TR-BME2 cells formed tube structures in the presence of bFGF, indicating maintenance of endothelial cell function, but not in its absence.

Conclusions:

• Basic fibroblast growth factor (bFGF) is essential for maintaining the endothelial progenitor cell (EPC) phenotype.
• bFGF actively suppresses the differentiation of EPCs into contractile smooth muscle cells (SMCs).
• These findings highlight bFGF's critical role in preserving EPC identity and endothelial potential.