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  

Oleh:

Yin-Lau, Lee ; Yuk-Ling, Chan ; Wan-Ngai, Chow ; Hung-Yu Ng, Ernest

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 91 no. 5 Sup (May 2009), page 2163-2171.
Topik: EG-VEGF; PKR1; PKR2; angiogenesis; cell-signaling pathways; UtMVEC-Myo

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2009.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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. Conclusion(s) : EG-VEGF has a direct angiogenic effect on UtMVEC-Myo that expresses EG-VEGF receptors (PKR1 and PKR2) and modulates cell proliferation and sprouting of the endothelial cells. It is suggested that EG-VEGF enhanced cell proliferation through the activation of MAPK pathway but not through the Akt pathway.

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