Are Mesenchymal Stem Cells So Bloody Great After All?

This Perspective discusses some activities of mesenchymal stem cells (MSCs) in the context of angiogenesis, focusing on contrasting effects that could call into question the extent to which MSCs can be used clinically in the future. We report on the antiangiogenic/antiproliferative effects of specific MSC populations (including bone marrow MSCs), their paracrine activity, tissue heterogeneity, and endothelial cell interactions. Also discussed are what could lead to contrasting effects of the influence of MSCs in regulating angiogenesis, pointing to some negative effects of these cells.

Maternal nutrition modifies trophoblast giant cell phenotype and fetal growth in mice.

Mammalian placentation is dependent upon the action of trophoblast cells at the time of implantation. Appropriate fetal growth, regulated by maternal nutrition and nutrient transport across the placenta, is a critical factor for adult offspring long-term health. We have demonstrated that a mouse maternal low-protein diet (LPD) fed exclusively during preimplantation development (Emb-LPD) increases offspring growth but programmes adult cardiovascular and metabolic disease.

Mouse early extra-embryonic lineages activate compensatory endocytosis in response to poor maternal nutrition.

Mammalian extra-embryonic lineages perform the crucial role of nutrient provision during gestation to support embryonic and fetal growth. These lineages derive from outer trophectoderm (TE) and internal primitive endoderm (PE) in the blastocyst and subsequently give rise to chorio-allantoic and visceral yolk sac placentae, respectively. We have shown maternal low protein diet exclusively during mouse preimplantation development (Emb-LPD) is sufficient to cause a compensatory increase in fetal and perinatal growth that correlates positively with increased adult-onset cardiovascular, metabolic and behavioural disease.