Functional consequences of prolactin signalling in endothelial cells: a potential link with angiogenesis in pathophysiology?
Bottom Line: These effects are blocked by a specific prolactin receptor antagonist, del1-9-G129R-hPRL.Interestingly, while prolactin has only little effect on endothelial cell proliferation, it markedly stimulates endothelial cell migration.Again, migration was reverted by del1-9-G129R-hPRL, indicating a direct effect of prolactin on its receptor.
Affiliation: Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. email@example.comShow MeSH
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Mentions: The angiogenic activity of prolactin was investigated in vivo using the early chicken embryo CAM assay. In control-treated embryos (0.9% NaCl), the capillary plexus was well developed and a homogeneous vascularization was observed (Fig. 2A). Topical administration of prolactin induced a clear change in the morphology of the vasculature (Fig. 2B). Digital analysis of the images did not reveal a change in the number of branching points: 1987(±58.87)/mm2 in the control condition versus 2124(±190.1)/mm2, P= 0.39, after addition of 1 μg prolactin and 2088(±85.71)/mm2, P= 0.34, after addition of 10 μg prolactin (Fig. 2D). By contrast, 10 μg prolactin induced a clear increase in vessel density compared to control [3683(±142.4)/mm2versus 3337(±36.5)/mm2, respectively, P= 0.0065; Fig. 2E], whilst addition of 1 μg prolactin had no effect on vessel density [3549(±340.2)/mm2, P= 0.42]. Combination of 1 μg prolactin with 10 μg of the prolactin receptor antagonist did not significantly affect the number of branching points [1885±(252.3)/mm2, P= 0.37; Fig. 2D] in comparison to the control condition. Additionally, prolactin plus antagonist did not influence the number of segments [3314±(398.0)/mm2, P= 0.85; Fig. 2E]. Moreover, prolactin enhanced the tortuosity of the vessels (Fig. 2B). The exposure to prolactin induced pillar formation and intussusceptive angiogenesis in the larger blood vessels (arrows in Fig. 2B), phenomena that are known to occur after exposure to the angiogenic growth factor VEGF [46, 47]. These effects of prolactin were markedly diminished by addition of the prolactin receptor antagonist del1-9-G129R-hPRL (Fig. 2C).
Affiliation: Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. firstname.lastname@example.org