Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats

Emilie Vomhof-DeKrey, Diane Darland, Ghribi Othman, Amy Bundy, James Roemmich, Kate Claycombe

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

A maternal low-protein (LP) diet in Sprague-Dawley rats results in low birth weight, rapid adipose tissue catch-up growth, adult obesity, and insulin resistance. The placenta functions to fulfill the fetus’ nutrient demands. Adequate angiogenic factor concentrations help to ensure normal growth and vasculature development of the placenta and, in turn, optimum maternal-to-fetal nutrient delivery. Maternal malnutrition creates a proinflammatory environment that leads to inhibition of placental tissue growth. Therefore, we hypothesized that a maternal LP diet will lead to abnormal angiogenesis via dysregulation of immune cells resulting in increased secretion of proinflammatory cytokines and reduced angiogenic factor expression. Sprague-Dawley dams were fed 8% LP or 20% normal protein diets for 3 weeks prior to breeding and throughout pregnancy. Placenta from dams fed a LP diet weighed less; had increased M2 macrophages producing TNFα, decreased M1 macrophages and iNKT cells; greater angiogenic factor (FGF2, VEGFR-1, IGF2) expression and protein content, and greater CD31/PECAM (platelet endothelial cell adhesion molecule) expression. Prenatal protein restriction may induce the placenta to upregulate compensatory mechanisms of angiogenesis in order to meet the nutrient demands of the fetus.

Original languageEnglish (US)
Pages (from-to)9-17
Number of pages9
JournalJournal of Reproductive Immunology
Volume118
DOIs
StatePublished - Nov 1 2016
Externally publishedYes

Fingerprint

Protein-Restricted Diet
Placenta
Sprague Dawley Rats
Angiogenesis Inducing Agents
Macrophages
Mothers
Food
Proteins
Fetus
Vascular Endothelial Growth Factor Receptor-1
Natural Killer T-Cells
Cell Adhesion Molecules
Low Birth Weight Infant
Fibroblast Growth Factor 2
Growth
Growth and Development
Malnutrition
Breeding
Insulin Resistance
Adipose Tissue

Keywords

  • Angiogenesis
  • Fibroblast growth factor
  • iNKT cells
  • Low protein diet
  • M1 and M2 macrophages

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats. / Vomhof-DeKrey, Emilie; Darland, Diane; Othman, Ghribi; Bundy, Amy; Roemmich, James; Claycombe, Kate.

In: Journal of Reproductive Immunology, Vol. 118, 01.11.2016, p. 9-17.

Research output: Contribution to journalArticle

@article{2188176d73964b068d64f6f642885eb3,
title = "Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats",
abstract = "A maternal low-protein (LP) diet in Sprague-Dawley rats results in low birth weight, rapid adipose tissue catch-up growth, adult obesity, and insulin resistance. The placenta functions to fulfill the fetus’ nutrient demands. Adequate angiogenic factor concentrations help to ensure normal growth and vasculature development of the placenta and, in turn, optimum maternal-to-fetal nutrient delivery. Maternal malnutrition creates a proinflammatory environment that leads to inhibition of placental tissue growth. Therefore, we hypothesized that a maternal LP diet will lead to abnormal angiogenesis via dysregulation of immune cells resulting in increased secretion of proinflammatory cytokines and reduced angiogenic factor expression. Sprague-Dawley dams were fed 8{\%} LP or 20{\%} normal protein diets for 3 weeks prior to breeding and throughout pregnancy. Placenta from dams fed a LP diet weighed less; had increased M2 macrophages producing TNFα, decreased M1 macrophages and iNKT cells; greater angiogenic factor (FGF2, VEGFR-1, IGF2) expression and protein content, and greater CD31/PECAM (platelet endothelial cell adhesion molecule) expression. Prenatal protein restriction may induce the placenta to upregulate compensatory mechanisms of angiogenesis in order to meet the nutrient demands of the fetus.",
keywords = "Angiogenesis, Fibroblast growth factor, iNKT cells, Low protein diet, M1 and M2 macrophages",
author = "Emilie Vomhof-DeKrey and Diane Darland and Ghribi Othman and Amy Bundy and James Roemmich and Kate Claycombe",
year = "2016",
month = "11",
day = "1",
doi = "10.1016/j.jri.2016.08.009",
language = "English (US)",
volume = "118",
pages = "9--17",
journal = "Journal of Reproductive Immunology",
issn = "0165-0378",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague-Dawley rats

AU - Vomhof-DeKrey, Emilie

AU - Darland, Diane

AU - Othman, Ghribi

AU - Bundy, Amy

AU - Roemmich, James

AU - Claycombe, Kate

PY - 2016/11/1

Y1 - 2016/11/1

N2 - A maternal low-protein (LP) diet in Sprague-Dawley rats results in low birth weight, rapid adipose tissue catch-up growth, adult obesity, and insulin resistance. The placenta functions to fulfill the fetus’ nutrient demands. Adequate angiogenic factor concentrations help to ensure normal growth and vasculature development of the placenta and, in turn, optimum maternal-to-fetal nutrient delivery. Maternal malnutrition creates a proinflammatory environment that leads to inhibition of placental tissue growth. Therefore, we hypothesized that a maternal LP diet will lead to abnormal angiogenesis via dysregulation of immune cells resulting in increased secretion of proinflammatory cytokines and reduced angiogenic factor expression. Sprague-Dawley dams were fed 8% LP or 20% normal protein diets for 3 weeks prior to breeding and throughout pregnancy. Placenta from dams fed a LP diet weighed less; had increased M2 macrophages producing TNFα, decreased M1 macrophages and iNKT cells; greater angiogenic factor (FGF2, VEGFR-1, IGF2) expression and protein content, and greater CD31/PECAM (platelet endothelial cell adhesion molecule) expression. Prenatal protein restriction may induce the placenta to upregulate compensatory mechanisms of angiogenesis in order to meet the nutrient demands of the fetus.

AB - A maternal low-protein (LP) diet in Sprague-Dawley rats results in low birth weight, rapid adipose tissue catch-up growth, adult obesity, and insulin resistance. The placenta functions to fulfill the fetus’ nutrient demands. Adequate angiogenic factor concentrations help to ensure normal growth and vasculature development of the placenta and, in turn, optimum maternal-to-fetal nutrient delivery. Maternal malnutrition creates a proinflammatory environment that leads to inhibition of placental tissue growth. Therefore, we hypothesized that a maternal LP diet will lead to abnormal angiogenesis via dysregulation of immune cells resulting in increased secretion of proinflammatory cytokines and reduced angiogenic factor expression. Sprague-Dawley dams were fed 8% LP or 20% normal protein diets for 3 weeks prior to breeding and throughout pregnancy. Placenta from dams fed a LP diet weighed less; had increased M2 macrophages producing TNFα, decreased M1 macrophages and iNKT cells; greater angiogenic factor (FGF2, VEGFR-1, IGF2) expression and protein content, and greater CD31/PECAM (platelet endothelial cell adhesion molecule) expression. Prenatal protein restriction may induce the placenta to upregulate compensatory mechanisms of angiogenesis in order to meet the nutrient demands of the fetus.

KW - Angiogenesis

KW - Fibroblast growth factor

KW - iNKT cells

KW - Low protein diet

KW - M1 and M2 macrophages

UR - http://www.scopus.com/inward/record.url?scp=84985026403&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84985026403&partnerID=8YFLogxK

U2 - 10.1016/j.jri.2016.08.009

DO - 10.1016/j.jri.2016.08.009

M3 - Article

VL - 118

SP - 9

EP - 17

JO - Journal of Reproductive Immunology

JF - Journal of Reproductive Immunology

SN - 0165-0378

ER -