Reduced maternal expression of adrenomedullin disrupts fertility, placentation, and fetal growth in mice
J. Clin. Invest. Manyu Li, et al. 116:2653 doi:10.1172/JCI28462 [Go to this article.]

Figure 4
FGR and developmental defects correlate with placentation and fetal AM genotype. (A) Timed matings were established for wild-type (white bar) and AM^+/– crosses (dark gray bar), and viable embryos were counted for gestational stages E9.5–E12.5. Severely growth restricted or resorbed embryos were included in the total litter size and are represented by the light gray area of the bars. *P < 0.001, viable embryos from AM^+/– intercrosses compared with viable embryos from wild-type crosses at the same gestational stage. (B) Representative E9.5 litter from AM^+/– intercross. The genotype of each embryo is indicated below. Note that growth restriction occurred in AM^+/– and AM^+/+ embryos. (C) Severe growth restriction and failure of neural tube closure in an AM^+/– embryo (right) compared with an AM^+/+ littermate (left) isolated at E9.5. (D) Moderate growth restriction and severe heart malformations in an AM^–/– embryo (right) compared with an AM^+/+ littermate (left) isolated at E9.5. (E) Expected outcomes and actual outcomes for genotypes of growth-restricted or abnormal embryos expressed as a percentage of total affected embryos. The smaller pie charts only include AM^+/– and AM^+/+ affected embryos. Data are representative of 35 AM^+/– litters examined at E9.5, which included 97 growth-restricted or malformed embryos.