Adler S, Chen X, Eng B
Department of Medicine, New York Medical College, Valhalla.
Kidney Int. 1990 Apr;37(4):1048-54. doi: 10.1038/ki.1990.84.
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-beta 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-beta sufficient to maximally inhibit growth had no effect on EGF binding to GEC. More prolonged exposure to TGF-beta, 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-beta released by inflammatory cells or platelets during the course of glomerular injury may play a role in modulating glomerular cell proliferation.
为了更好地了解可能刺激肾小球内皮细胞（GEC）增殖的体内因素，研究了培养的大鼠GEC1与几种生长因子的相互作用。GEC对表皮生长因子（EGF）有反应而增殖，但对胰岛素样生长因子-1（IGF-1）、巨噬细胞刺激活性（MSA）或血小板衍生生长因子（PDGF）无反应。在利用125I-EGF进行的饱和及竞争结合研究中检测到了EGF的特异性、可饱和受体，其解离常数（Kd）约为1.7 nM，每个细胞有86,000个结合位点。转化生长因子-β（TGF-β）以时间和剂量依赖的方式抑制GEC生长，短暂的早期暴露会导致长期的生长抑制，且这种抑制不能被EGF逆转。足以最大程度抑制生长的TGF-β暴露对EGF与GEC的结合没有影响。然而，更长时间暴露于TGF-β确实导致GEC上EGF受体的表观数量增加，但Kd没有变化。这些研究表明，在肾小球损伤过程中由炎症细胞或血小板释放的EGF和TGF-β可能在调节肾小球细胞增殖中起作用。
