Skip to main content
ARS Home » Plains Area » Clay Center, Nebraska » U.S. Meat Animal Research Center » Livestock Bio-Systems » Research » Publications at this Location » Publication #372382

Research Project: Improving Lifetime Productivity in Swine

Location: Livestock Bio-Systems

Title: Uterine gland development and FOXA2 immunolocalization in gilts at postnatal 14 affected by lactocrine deficiency from birth

item PARANJPE, NINA - Rutgers University
item HO, TEH-YUAN - Rutgers University
item WILEY, ANNE - Auburn University
item Oliver, William
item Miles, Jeremy
item Lents, Clay
item BARTOL, FRANK - Auburn University
item BAGNELL, CAROL - Rutgers Agriculture Research & Extension Center

Submitted to: Society for the Study of Reproduction Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 4/28/2020
Publication Date: 7/12/2020
Citation: Paranjpe, N.E., Ho, T., Wiley, A.A., Oliver, W.T., Miles, J.R., Lents, C.A., Bartol, F.F., Bagnell, C.A. 2020. Uterine gland development and FOXA2 immunolocalization in gilts at postnatal 14 affected by lactocrine deficiency from birth [abstract]. Society for the Study of Reproduction Annual Meeting, Virtual. p. 245. Abstract 1929. Available:

Interpretive Summary:

Technical Abstract: Bioactive factors of maternal origin present in colostrum are delivered into the neonatal circulation via a lactocrine mechanism and affect patterns of uterine development in swine with lasting consequences. Imposition of a lactocrine null condition by experimental milk replacer feeding for two days from birth (postnatal day = PND 0) altered uterine gene expression patterns globally by PND 2 and inhibited uterine gland development by PND 14. Colostrum consumption can be measured in nursing gilts by monitoring neonatal serum immunoglobin immunocrit ratio (iCrit). Lactocrine deficiency, defined as low iCrit at birth, altered uterine development by PND 14 as reflected by reduced glandular epithelial (GE) and stromal cell proliferation. Lactocrine deficiency from birth impairs lifetime fecundity in adults, indicated by reduced live litter size. Here, objectives were to determine effects lactocrine deficiency from birth on endometrial morphology, uterine gland development and forkhead homeobox A2 (FOXA2) immunostaining patterns on PND 14. FOXA2, a transcription factor essential for the differentiation and development of uterine glands, marks uterine GE cells in humans, mice and sheep, but has not been reported in pigs. In this study crossbred gilts were assigned to low (n = 12) or high (n = 10) iCrit groups based on iCrit ratio values determined on PND 0. Serum iCrit ratios were greater (P<0.01) in high (12.04 ± 0.27 relative units) versus low (1.92 ± 0.27 relative units) iCrit groups, indicating a difference in colostrum consumption between groups of approximately 6-fold at birth. Endometrial development was quantified histomorphometrically and FOXA2 expression localized in uterine GE cells immunohistochemically in a subset of high versus low iCrit gilts (6 litter-matched gilts per group) on PND14 when uterine tissues were collected. Neither birth weights, PND 14 body weights, ovary weights nor uterine weights differed between groups. However, both the number of GE cells/mm2 (P<0.05) and, to a lesser extent, endometrial thickness (P<0.08) were reduced in low as compared to high iCrit gilts. Uterine gland penetration depth did not differ between the two groups. Immunoreactive FOXA2 protein was localized consistently and uniquely in GE cells of both low and high iCrit gilts at PND14. The increased number of uterine GE cells/mm2 in high iCrit gilts indicated an overall increase in FOXA2 expression. Results indicate that lactocrine deficiency from birth alters endometrial development resulting in fewer GE cells and an associated decrease in overall expression of FOXA2. Reduction in endometrial FOXA2 expression may contribute to alterations in neonatal lactocrine programing of uterine tissues. Results reinforce the idea that lactocrine deficiency in nursing gilts, maintained under normal husbandry conditions, affects patterns of neonatal uterine endometrial development. Such changes in the neonatal uterine organizational program can affect fecundity in adulthood. [Support: USDA-NIFA 2013-67016-20523]