CONTROL OF RAT GLOMERULAR EPITHELIAL-CELL GROWTH-INVITRO

The interaction of cultured rat GEC1 with several growth factors was explored in order to obtain a better understanding of in vivo factors which might stimulate GEC proliferation. GEC proliferated in response to EGF but not IGF-1, MSA or PDGF. Specific, saturable receptors for EGF were detected in saturation and competition binding studies utilizing 125I-EGF with an approximate Kd of 1.7 nM and 86.000 binding sites per cell. TGF-β inhibited GEC growth in a time and dose dependent manner with a brief early exposure resulting in prolonged growth inhibition which was not reversible by EGF. Exposure to TGF-β sufficient to maximally inhibit growth had no effect on EGF binding to GEC. More prolonged exposure to TGF-β, however, did result in an increase in the apparent number of EGF receptors on GEC but no change in Kd. These studies suggest that EGF and TGF-β released by inflammatory cells or platelets during the course of glomerular injury may play a role in modulating glomerular cell proliferation.