Regulation of Prolactin Transformation in the Rat Pituitary

Grosvenor, Clark E.; Mena, Flavio

doi:10.1002/9780470514283.ch6

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…By contrast, such relationships are less obvious in eutherian mammals, in which a single major change in milk composition is defined by the transition from production of colostrum (first milk) to milk early in lactation [2]. Still, peptide MbFs traverse the immature gastrointestinal (GI) tract and are delivered into the neonatal circulation [16][17][18]. It is clear that colostrum serves as a conduit for lactocrine transmission of signaling molecules [1,9,[18][19][20][21][22][23][24][25].…”

Section: Introductionmentioning

confidence: 98%

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

Miller

Wiley

Chen

et al. 2013

Biology of Reproduction

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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.

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Section: Introductionmentioning

confidence: 98%

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

Miller

Wiley

Chen

et al. 2013

Biology of Reproduction

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“…The PIFs include dopamine, gonadotropin‐combined peptide, and melanocyte stimulating hormone. 14 , 15 PRFs include thyroid stimulating hormone releasing hormone (TRH), gonadotropin‐releasing hormone (GnRH), angiotensin II, and vasoactive peptide. 16 As the most important PIFs, dopamine inhibits the secretion of pPRL via the type 2 dopamine receptor on the surface of lactotroph cells.…”

Section: Secretion and Regulation Of Prlmentioning

confidence: 99%

“…9 After cleavage of the 28 amino acid signal peptides, the mature protein containing 199 residues is depicted as the 23-kDa PRL monomer. In addition, numerous variants of PRL have been identified, including big PRL (dimer of the monomeric form), big-big PRL (complexes of monomeric form and IgG autoantibodies), and some variants with smaller molecular weight (14,16,. As shown in Figure 1, a number of variants with a molecular weight between 5.6 10 and 18 kDa are defined as a novel family 11 and named vasoinhibins, as these peptides share blood vessel inhibitory properties.…”

Section: Molecul Ar Forms Of Prlmentioning

confidence: 99%

“…As shown in Figure 2, pPRL is mainly synthesized and secreted by the lactotroph cells of the anterior pituitary, 8,9 and this process is regulated by a number of prolactin‐releasing factors (PRFs) and prolactin‐inhibiting factors (PIFs) 13 released from the hypothalamus. The PIFs include dopamine, gonadotropin‐combined peptide, and melanocyte stimulating hormone 14,15 . PRFs include thyroid stimulating hormone releasing hormone (TRH), gonadotropin‐releasing hormone (GnRH), angiotensin II, and vasoactive peptide 16 .…”

Section: Secretion and Regulation Of Prlmentioning

confidence: 99%

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The role of prolactin/vasoinhibins in cardiovascular diseases

Zhao

Gong

Shi³

et al. 2022

Anim Models and Exp Med

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Prolactin (PRL) is a polypeptide hormone that is mainly synthesized and secreted by the lactotroph cells of the pituitary. There are two main isoforms of PRL: 23‐kDa PRL (named full‐length PRL) and vasoinhibins (including 5.6–18 kDa fragments). Both act as circulating hormones and cytokines to stimulate or inhibit vascular formation at different stages and neovascularization, including endothelial cell proliferation and migration, protease production, and apoptosis. However, their effects on vascular function and cardiovascular diseases are different or even contrary. In addition to the structure, secretion regulation, and signal transduction of PRL/vasoinhibins, this review focuses on the pathological mechanism and clinical significance of PRL/vasoinhibins in cardiovascular diseases.

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What can we Learn from Sampling Hypophysial Portal Blood?

Clarke¹

2007

Novartis Foundation Symposia

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Regulation of Prolactin Transformation in the Rat Pituitary

Cited by 5 publications

References 33 publications

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

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

The role of prolactin/vasoinhibins in cardiovascular diseases

What can we Learn from Sampling Hypophysial Portal Blood?

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