Perinatal imprinting by estrogen and adult prostate disease
- Department of Woman and Child Health, Pediatric Endocrinology Unit, Astrid Lindgren Children's Hospital, Karolinska Institute and University Hospital, SE17176 Stockholm, Sweden
One of the major conceptual novelties in human medicine emerging during the last two decades is the fetal-origin hypothesis, challenging our traditional view on the pathogenesis of common chronic disorders. This hypothesis, originally put forward by Barker et al. (1), states that prenatal events, mainly of nutritional and metabolic nature, are memorized (“imprinted”) by the developing organism and, if inappropriate for the postnatal situation, may result in the development of diseases during the adult age. Although intriguing and supported by an increasing number of experimental and epidemiological studies, the “Barker hypothesis” must still be validated with respect to its underlying biology. In this issue of PNAS, Omoto et al. (2) reveal that a well tuned temporal and spatial expression of estrogen receptor α (ERα) and ERβ in the epithelial and stromal cells of the ventral prostate, concomitant with an estrogen signal, is required for normal morphological development of the prostate in mice. By employing ERα and ERβ gene-deleted mice, it was shown that ERα, but not ERβ, is necessary for the neonatal imprinting …
