Vascular Repair After Menstruation Involves Regulation of Vascular Endothelial Growth Factor-Receptor Phosphorylation by sFLT-1

Michael D. Graubert, Graubert MD, Ortega MA, Maria-Asunción Ortega, Bruce Kessel, Mortola JF, Joseph F. Mortola, Iruela-Arispe ML, M. Luisa Iruela‐Arispe
The American Journal of Pathology · 2001 · vol. 158(4) , pp. 1399–1410 · doi:10.1016/s0002-9440(10)64091-6 · PMID:11290558 · PMC1891924 · W2005577087
article OA: bronze CC0 ⤵ 12 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This paper investigates the role of soluble fms-like tyrosine kinase-1 (sFLT-1) in vascular repair after menstruation, specifically focusing on its regulation of vascular endothelial growth factor-receptor phosphorylation.

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Abstract

Regeneration of the endometrium after menstruation requires a rapid and highly organized vascular response. Potential regulators of this process include members of the vascular endothelial growth factor (VEGF) family of proteins and their receptors. Although VEGF expression has been detected in the endometrium, the relationship between VEGF production, receptor activation, and endothelial cell proliferation during the endometrial cycle is poorly understood. To better ascertain the relevance of VEGF family members during postmenstrual repair, we have evaluated ligands, receptors, and activity by receptor phosphorylation in human endometrium throughout the menstrual cycle. We found that VEGF is significantly increased at the onset of menstruation, a result of the additive effects of hypoxia, transforming growth factor-alpha, and interleukin-1beta. Both VEGF receptors, FLT-1 and KDR, followed a similar pattern. However, functional activity of KDR, as determined by phosphorylation studies, revealed activation in the late menstrual and early proliferative phases. The degree of KDR phosphorylation was inversely correlated with the presence of sFLT-1. Endothelial cell proliferation analysis in endometrium showed a peak during the late menstrual and early proliferative phases in concert with the presence of VEGF, VEGF receptor phosphorylation, and decrease of sFLT-1. Together, these results suggest that VEGF receptor activation and the subsequent modulation of sFLT-1 in the late menstrual phase likely contributes to the onset of angiogenesis and endothelial repair in the human endometrium.

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organisms 12
human human yellowmouth grouper human cucumber mosaic virus, cmv renilla rabbits transgenic mice red junglefowl naine d'afrique de l'ouest noordeloos 2009062 primates
chemicals 31
hormone estradiol progesterone luteinizing hormone formaldehyde polyaniline polymer dextran sulfate 11 hydroxy-(14r,15s)-epoxy-(5z,8z,12e)-icosatrienoate ethylenediaminetetraacetic acid phenol cyanoguanidine isothiocyanate agarose penicillin streptomycin amikacin steroid calcein red-orange oxygen glycerol triton fluoride leupeptin pepstatin a heparin sodium metavanadate sucrose o(4)-phosphotyrosine sex hormone estrogen steroid

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