Nursing for 48 Hours from Birth Supports Porcine Uterine Gland Development and Endometrial Cell Compartment-Specific Gene Expression1

Abstract

The first 2 wk of neonatal life constitute a critical period for estrogen receptor alpha (ESR1)-dependent uterine adenogenesis in the pig. A relaxin receptor (RXFP1)-mediated, lactocrine-driven mechanism was proposed to explain how nursing could regulate endometrial ESR1 and related gene expression events associated with adenogenesis in the porcine neonate during this period. To determine effects of nursing on endometrial morphogenesis and cell compartment-specific gene expression, gilts (n = 6-8/group) were assigned at birth to be either 1) nursed ad libitum for 48 h, 2) gavage fed milk replacer for 48 h, 3) nursed ad libitum to Postnatal Day (PND) 14, or 4) gavage fed milk replacer for 48 h followed by ad libitum nursing to PND 14. Uteri were collected on PND 2 or PND 14. Endometrial histoarchitecture and both ESR1 and proliferating cell nuclear antigen (PCNA) labeling indexes (LIs) were evaluated. Laser microdissection was used to capture epithelium and stroma to evaluate treatment effects on cell compartment-specific ESR1, VEGFA, and RXFP1 expression. Imposition of a lactocrine-null state by milk replacer feeding for 48 h from birth retarded endometrial development and adenogenesis. Effects of replacer feeding, evident by PND 2, were marked by PND 14 when endometrial thickness, glandularity, and gland depth were reduced. Consistently, in lactocrine-null gilts, PCNA LI was reduced in glandular epithelium (GE) and stroma on PND 14, when epithelial ESR1 expression and ESR1 LI in GE were reduced and stromal VEGFA and RXFP1 expression increased. Results establish that lactocrine signaling effects morphogenetic changes in developing uterine tissues that may determine reproductive capacity later in life.

Relationships between day one piglet serum immunoglobulin immunocrit and subsequent growth, puberty attainment, litter size, and lactation performance1

“…Previous reports indicate that along with gut development, ingestion of colostrum promotes early neonatal developmental events in uterine and testis development (Frankshun et al, 2012;Miller et al, 2013;Rahman et al, 2014). Specifically, lack of colostrum delays the onset of uterine gland development and delays hallmarks of uterine gland development such as the elaboration of estrogen receptor expression and matrix metalloproteases in neonatal uterine tissues Frankshun et al, 2012;Miller et al, 2013). Administration of exogenous relaxin, which is a component of colostrum (Frankshun et al, 2009, can duplicate many of the effects of colostrum but not all of them Yan et al, 2005Yan et al, , 2008Masters et al, 2007;Bartol et al, 2009).…”

The role of genetics in estrogen responses: a critical piece of an intricate puzzle

“…123). The molecular events associated with lactocrine signaling to the neonate, and subsequent uterine development, are well-established in pigs (117,124). In addition, nonobese diabetic mice have different risks of developing autoimmune type 1 diabetes depending on the strain of their foster mothers, representing a clear example of gene-by-maternal postnatal environment effects influencing adult-onset autoimmune disease (119).…”

Duration of breastfeeding is associated with emotional eating through its effect on alexithymia in boys, but not girls

“…The possibility that oxytocin in breast milk shapes the phenotype of the offspring would fit in the Lactocrine Programming hypothesis (Bartol, Wiley, & Bagnell, 2009;Miller, Wiley, Chen, Bagnell, & Bartol, 2013). Accumulating evidence from animal studies suggests that maternal hormones, ingested through breast milk, affect offspring development in a sex-specific manner (Angelucci, Patacchioli, Chierichetti, & Laureti, 1983;Casolini et al, 1997;Catalani et al, 2002;Hinde et al, 2014;Sullivan, Hinde, Mendoza, & Capitanio, 2011).…”