Physiological roles of insulin-like growth factor binding protein 3 in mouse endometrium

IGFBP3抑制igf1诱导的子宫内膜细胞增殖。雌二醇-17β(E2)和TGFα可降低Igfbp3 mRNA在子宫内膜基质细胞中的表达。MMP3和Kallikrein (Klk) 1降解IGFBP3。TGFα使Mmp3mRNA表达增加，E2使Klk1mRNA表达增加。增强的MMP3和Klk1的产生降低了子宫内膜中IGFBP3的水平，导致游离IGF1水平升高。E2增加Igf1mRNA的表达。这些发现提供了E2刺激IGF1产生，而E2和tgf α降低IGFBP3水平，从而刺激子宫内膜间质细胞增殖的可能调控机制。

IGFBP3 inhibited IGF1-induced proliferation of endometrial cells. Igfbp3 mRNA expression in the endometrial stromal cells was decreased by estradiol-17β(E2) and TGFα.MMP3 and Kallikrein (Klk) 1 degrade IGFBP3. Mmp3mRNA expression was increased by TGFα, and Klk1mRNA expression was by E2. Enhanced production of MMP3 and Klk1 decrease IGFBP3 levels in the endometrium, resulting in the increase in free IGF1 levels. E2 increased Igf1mRNA expression.These findings provide the possible regulatory mechanism of endometrialstromal cell proliferation that E2 stimulates IGF1 production, while E2 and TGFαdecrease IGFBP3 level, leading to the stimulation of endometrial cell proliferation.