Fetal growth at term was unaffected [5]. This study clearly shows that labyrinthine trophoblast plays a role in regulating fetoplacental arterial tree development although the precise mechanisms remain to be elucidated. The fetoplacental arterial vasculature of the mouse is much simpler than

that of the human, which makes it a more tractable model, but it is also strikingly similar. In both species, the umbilical vessels normally supply a discoid, hemochorial placenta from a central location [15, 37, 1, 6], from which the chorionic arteries branch across the fetal-facing surface of the placenta although in the human there MK-1775 supplier are two umbilical arteries versus one in the mouse. In both species, the fetoplacental arterial trees branch from these superficial chorionic arteries

to branch deeply into the exchange region of the placenta. However, in the human there are ~20 fetoplacental arterial trees each supplying a cotyledon Angiogenesis inhibitor whereas there is only one tree in the mouse. Even so, the fetoplacental arterial branching structure in a single human cotyledon is much more elaborate than the mouse (Figure 7). The large size of the human cotyledon currently limits the resolution that can be achieved by micro-CT imaging. Higher resolution can be obtained by decreasing the size of the specimen. This was performed previously on 2 mm cores through human placentas, in which arteries, capillaries, and veins had been filled with contrast agent [23]. Specimens were imaged at 8 μm resolution permitting at least partial pentoxifylline detection of capillaries. A total vascular volume fraction of 20% was calculated for healthy controls compared to 8% in placentas from fetuses with growth restriction [23]. Vessel tracking and detailed analysis of the tree was not performed. Comparison

with the human placenta highlights a major advantage for studying factors controlling growth and development of the fetoplacental arterial tree in the mouse model, the small size of the placenta (~100 μL) [9]. The small sample size facilitates the acquisition of 3D information at high resolution for the whole vascular tree thereby maintaining connectivity information and also obviating the need to scale up to the whole organ. A smaller tissue volume also means a simpler tree since fewer generations of branching are required to supply the whole organ thereby simplifying vessel tracking and quantitative analysis (e.g., Figure 7). There are additional advantages for studying the fetoplacental mouse model. The fetoplacental arterial tree grows into a fairly homogeneous spongy labyrinth filled with finely divided sinusoids perfused by maternal blood. Thus, the structure of the tree is not constrained by other anatomic features such as chambers (e.g., heart) (data not shown) or airways (e.g., lung), lobes (e.g., brain), or layers (e.g.