Endocrine gland-derived vascular endothelial growth factor stimulates proliferation and tube formation in human uterine microvascular endothelial cell through the mitogen-activated protein kinase but not through the Akt pathway

内分泌腺源性血管内皮生长因子通过丝裂原活化蛋白激酶而不是 Akt 通路刺激人子宫微血管内皮细胞增殖和管形成

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作者:Yin-Lau Lee, Yuk-Ling Chan, Wan-Ngai Chow, Ernest Hung-Yu Ng, Kai-Fai Lee, William S B Yeung, Pak-Chung Ho

Objective

To study the angiogenic functions of endocrine gland-derived vascular endothelial growth factor (EG-VEGF) on a normal myometrial uterine microvascular endothelial cell line (UtMVEC-Myo) and the signaling pathways elicited by EG-VEGF in UtMVEC-Myo. Design: Experimental laboratory study. Setting: University gynecology unit. Patient(s): Infertile women undergoing diagnostic laparoscopy for assessment of tubal patency. Intervention(s): Real-time polymerase chain reaction (PCR) analysis of mRNA of EG-VEGF and its receptors, PKR1 and PKR2, in UtMVEC-Myo and endometrial samples. The effects of EG-VEGF on the cell proliferation, tube formation, and cell signaling pathways of UtMVEC-Myo were studied. Main outcome measure(s): Cell proliferation, tube formation, and molecules of cell-signaling pathways in the treated UtMVEC-Myo. Result(s): UtMVEC-Myo cells had PKR1 and PKR2 but not EG-VEGF mRNA. EG-VEGF significantly stimulated cell proliferation and tube formation in UtMVEC-Myo cells. EG-VEGF activated p44/42 mitogen-activated protein kinase (MAPK) but not Akt signaling pathway. The effects of EG-VEGF on p44/42 MAPK phosphorylation and cell proliferation were nullified by the specific MAPK inhibitor, PD98059.

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