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TROPHOBLAST REGULATION OF MATERNAL BLOOD FLOW.
Cross, James1, Hemberger, Myriam1, Lu, Yong 2, Nozaki, Tadashige 3, Whiteley, Kathie 2, Masutani, Mitsuko 3, Adamson, Lee 2, 1 2 3
ABSTRACT- The vascular bed of the uterus changes dramatically during pregnancy as new vessels form and then become modified such that maternal blood comes in direct contact with trophoblast cells on the placental surface. To address the role of trophoblast cells in regulating maternal vessel development, we first described blood flow through the mouse placenta by preparing vascular casts and serial histological sections. Cytokeratin immunoreactivity and PAS-positive granules were used as markers to identify the location of trophoblast cells and uNK cells, respectively. The mature circulatory pattern is established by embryonic day (E) 9.5. The uterine artery branches into several smaller arteries at the mesometrial triangle of each implantation site. The arteries that traverse the decidua are initially in close proximity to uNK cells, have spiral shape and lack laminated smooth muscle layers. Loss of vascular smooth muscle in decidual arteries likely promotes vasodilation and therefore increased blood flow. uNK cells are known to be essential for vasodilation in this region, but our finding of a lack of trophoblast cells suggests that they have no role. The spiral arteries converge at the trophoblast giant cell layer, which is the outermost layer of the placenta up to E10.5, to form 1-4 large canals that carry blood into the labyrinth. The arteries lose their endothelium once they contact the giant cell layer. Two types of trophoblast invasion were observed after this basic structure was established. Peri-arteriolar migration of trophoblast giant cells was observed between E10.5 and 12.5. Interstitial invasion of decidua was also observed, but only by E14.5 and by glycogen trophoblast cells. We hypothesize that local factors released by trophoblast giant cells control many of the striking structural features of this unique vascular bed. We have addressed this by examining their detailed expression of angiogenic factors (Vegf, proliferin/Plf), anti-angiogenic factors (soluble Flt1, proliferin-related protein/Plfr) and vasoactive substances (adrenomedulliin/Adm, eNOS, iNOS). Supported by grants from the CIHR.
KEY WORDS: trophoblast, angiogenesis, implantation
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