Pregnancy and lactation modulate maternal splenic growth and development of the erythroid lineage in the rat and mouse

Abstract

Maternal physiology changes dramatically during the course of gestation and lactation to meet the needs of the developing fetus and newborn. In the present study, we examined the influence of pregnancy and lactation on growth and erythroid gene expression patterns of the maternal spleen. Holtzman Sprague-Dawley rats and CD-1 mice were killed at various stages of gestation and post partum. We observed pregnancy dependent increases in spleen weight and spleen DNA content in both the rat and mouse. In the rat, spleen size was greatest at the end of pregnancy and regressed post partum. In contrast, mouse spleen size peaked by gestational Day 13 and regressed to its non-pregnant weight before parturition. Pregnancy dependent changes in the size of the spleen were primarily due to an increase in red pulp. Maternal spleen expression of erythroid-associated genes (erythroid Krüppel-like factor, erythroid 5-aminolevulinate synthase-2, beta-major globin) was influenced by pregnancy and lactation. A pregnancy dependent increase in erythroid progenitors was also observed. In summary, the demands of pregnancy and lactation cause marked adaptations in the maternal spleen. The maternal spleen increases in size and exhibits an expansion of the erythroid lineage.

Enlargement of the spleen as an incidental finding on CT in post-partum females with fever

“…In the current study, based on CT, post-partum splenomegaly concurs with the previously recorded gradual increase in size of the spleen during pregnancy found on ultrasound [1]. Although we could find no other studies in humans, splenomegaly has been documented in pregnant rats with up to a 50% increase in weight [11,12]. These maternal rat spleens regress post partum to their non-pregnant weight [11].…”

“…Although we could find no other studies in humans, splenomegaly has been documented in pregnant rats with up to a 50% increase in weight [11,12]. These maternal rat spleens regress post partum to their non-pregnant weight [11].…”

Nrf2 Participates in Regulating Maternal Hepatic Adaptations to Pregnancy

“…Pregnancy is characterized by a series of coordinated physiological adjustments in major maternal organ systems to meet the metabolic demands of the development and growth of the placenta and fetus (Smith et al, 1998;Nielsen et al, 1999;Audus et al, 2002;Shingo et al, 2003;Sweeney et al, 2006;Bustamante et al, 2008;Huang et al, 2009;Kim et al, 2010). Among the maternal adaptive responses to pregnancy is the enlargement of the maternal liver, which has previously been described in several reports (Kennaway and Kennaway, 1944;Kennedy et al, 1958;Smith, 1975;Mesbah and Baldwin, 1983;Hollister et al, 1987;Dickmann et al, 2008).…”

Pregnancy Alters the Proliferation and Apoptosis of Mouse Splenic Erythroid Lineage Cells and Leukocytes1

“…The production of erythrocytes in the murine spleen is augmented during pregnancy [4][5][6] and may be mediated by erythropoietin (EPO) signaling [7][8][9]. A recent study demonstrated that the proportion of erythrocyte precursors in the murine spleen expands during midgestation [10]. However, this study did not address the effects this increase in erythroid cells had on other populations in the spleen.…”