Signaling pathway for the regulation of dNKs at the maternal-fetal interface via collagen/LAIR-1 interaction

Increased ERK1/2 phosphorylation (P-ERK1/2) is involved in endothelial progenitor cell (angioblast) differentiation and proliferation in endometriosis. Several individual cells (asterisks) and cell clusters of vascular like structures (presumptive vessels; arrows) display the strongest P-ERK1/2 immunoreactivity in the ectopic endometrium, whereas endothelial cells in distal to ectopic tissue (arrowheads) exhibit weak to moderate P-ERK1/2 immunoreactivity (A, B). CD34, an angioblast marker and P-ERK1/2 double immunostaining is seen in ectopic endometrial specimens (C-E) with stronger P-ERK1/2 (brown) immunoreactivity in CD34 immunoreactive (red) endothelial progenitor cells (arrows; C or D) vs. mature vascular endothelial cells (arrowheads in C or E). Representative photomicrographs of CD34 and PCNA double immunostained ectopic endometrial specimens display stronger co-expression of CD34 (red) and PCNA (brown) in endothelial progenitor cells (arrows; F) than in mature vascular endothelial cells (arrowheads; G), indicating proliferative nature of this CD34 immunoreactive angioblasts.