Placental structural abnormalities have detrimental hemodynamic consequences in a rat model of maternal hyperglycemia

Lehtoranta Lara, Vuolteenaho Olli, Laine Jukka, Polari Lauri, Ekholm Eeva, Juha Rasanen

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Introduction Human type 1 diabetic pregnancy is associated with placental structural and hemodynamic abnormalities. We hypothesized that in rat fetuses of hyperglycemic dams, placental and fetal blood flow velocity waveforms demonstrate compromised hemodynamics when compared to control fetuses, and these hemodynamic parameters correlate with placental structural abnormalities at near term gestation. Methods Streptozotocin-induced maternal hyperglycemia group comprised 10 dams with 107 fetuses and the control group 20 dams with 219 fetuses. Doppler-ultrasonographic examinations were performed at gestational days 13-14, 16-17, and 19-21. After the last examination, placentas were collected for morphologic, gene expression, and cytokine analysis. Results Umbilical artery (UA), descending aorta (DAO), and ductus venosus (DV) pulsatility indices (PI) were significantly higher at each study point in maternal hyperglycemia compared to controls. Placental size, glycogen storages, venous thrombosis formation, and fluid accumulation were increased in maternal hyperglycemia. Epidermal growth factor receptor (Edgfrb), platelet derived growth factor receptor beta polypeptide (Pdgfrb), and tumor necrosis factor receptor superfamily, member 12α (Tnfrsf12α) expressions were decreased. Interleukin (IL) -2 and -4 concentrations were decreased, and IL-1beta levels were increased in maternal hyperglycemia. UA PIs correlated positively with DV PIV, DAO PI, fluid accumulation, and glycogen storages. UA PIs correlated negatively with IL-4, Edgfrb, and Pdgfrb. Discussion In maternal hyperglycemia, placental and fetal hemodynamics were compromised during the last trimester of pregnancy compared to normoglycemic pregnancies. Placental structural, metabolic, and growth related gene expression, and inflammatory marker abnormalities were associated with hemodynamic compromise.

Original languageEnglish (US)
Pages (from-to)54-60
Number of pages7
JournalPlacenta
Volume44
DOIs
StatePublished - Aug 1 2016
Externally publishedYes

Fingerprint

Hyperglycemia
Hemodynamics
Mothers
Umbilical Arteries
Fetus
Platelet-Derived Growth Factor beta Receptor
Pregnancy
Thoracic Aorta
Glycogen
Interleukin-4
Gene Expression
Peptides
Blood Flow Velocity
Tumor Necrosis Factor Receptors
Third Pregnancy Trimester
Streptozocin
Fetal Blood
Interleukin-1beta
Epidermal Growth Factor Receptor
Venous Thrombosis

Keywords

  • Animal model
  • Circulation
  • Impedance
  • Maternal hyperglycemia
  • Placenta

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Reproductive Medicine
  • Developmental Biology

Cite this

Placental structural abnormalities have detrimental hemodynamic consequences in a rat model of maternal hyperglycemia. / Lara, Lehtoranta; Olli, Vuolteenaho; Jukka, Laine; Lauri, Polari; Eeva, Ekholm; Rasanen, Juha.

In: Placenta, Vol. 44, 01.08.2016, p. 54-60.

Research output: Contribution to journalArticle

Lara, Lehtoranta ; Olli, Vuolteenaho ; Jukka, Laine ; Lauri, Polari ; Eeva, Ekholm ; Rasanen, Juha. / Placental structural abnormalities have detrimental hemodynamic consequences in a rat model of maternal hyperglycemia. In: Placenta. 2016 ; Vol. 44. pp. 54-60.
@article{56e0b1a63587497d9bbd4128eac95e34,
title = "Placental structural abnormalities have detrimental hemodynamic consequences in a rat model of maternal hyperglycemia",
abstract = "Introduction Human type 1 diabetic pregnancy is associated with placental structural and hemodynamic abnormalities. We hypothesized that in rat fetuses of hyperglycemic dams, placental and fetal blood flow velocity waveforms demonstrate compromised hemodynamics when compared to control fetuses, and these hemodynamic parameters correlate with placental structural abnormalities at near term gestation. Methods Streptozotocin-induced maternal hyperglycemia group comprised 10 dams with 107 fetuses and the control group 20 dams with 219 fetuses. Doppler-ultrasonographic examinations were performed at gestational days 13-14, 16-17, and 19-21. After the last examination, placentas were collected for morphologic, gene expression, and cytokine analysis. Results Umbilical artery (UA), descending aorta (DAO), and ductus venosus (DV) pulsatility indices (PI) were significantly higher at each study point in maternal hyperglycemia compared to controls. Placental size, glycogen storages, venous thrombosis formation, and fluid accumulation were increased in maternal hyperglycemia. Epidermal growth factor receptor (Edgfrb), platelet derived growth factor receptor beta polypeptide (Pdgfrb), and tumor necrosis factor receptor superfamily, member 12α (Tnfrsf12α) expressions were decreased. Interleukin (IL) -2 and -4 concentrations were decreased, and IL-1beta levels were increased in maternal hyperglycemia. UA PIs correlated positively with DV PIV, DAO PI, fluid accumulation, and glycogen storages. UA PIs correlated negatively with IL-4, Edgfrb, and Pdgfrb. Discussion In maternal hyperglycemia, placental and fetal hemodynamics were compromised during the last trimester of pregnancy compared to normoglycemic pregnancies. Placental structural, metabolic, and growth related gene expression, and inflammatory marker abnormalities were associated with hemodynamic compromise.",
keywords = "Animal model, Circulation, Impedance, Maternal hyperglycemia, Placenta",
author = "Lehtoranta Lara and Vuolteenaho Olli and Laine Jukka and Polari Lauri and Ekholm Eeva and Juha Rasanen",
year = "2016",
month = "8",
day = "1",
doi = "10.1016/j.placenta.2016.06.002",
language = "English (US)",
volume = "44",
pages = "54--60",
journal = "Placenta",
issn = "0143-4004",
publisher = "W.B. Saunders Ltd",

}

TY - JOUR

T1 - Placental structural abnormalities have detrimental hemodynamic consequences in a rat model of maternal hyperglycemia

AU - Lara, Lehtoranta

AU - Olli, Vuolteenaho

AU - Jukka, Laine

AU - Lauri, Polari

AU - Eeva, Ekholm

AU - Rasanen, Juha

PY - 2016/8/1

Y1 - 2016/8/1

N2 - Introduction Human type 1 diabetic pregnancy is associated with placental structural and hemodynamic abnormalities. We hypothesized that in rat fetuses of hyperglycemic dams, placental and fetal blood flow velocity waveforms demonstrate compromised hemodynamics when compared to control fetuses, and these hemodynamic parameters correlate with placental structural abnormalities at near term gestation. Methods Streptozotocin-induced maternal hyperglycemia group comprised 10 dams with 107 fetuses and the control group 20 dams with 219 fetuses. Doppler-ultrasonographic examinations were performed at gestational days 13-14, 16-17, and 19-21. After the last examination, placentas were collected for morphologic, gene expression, and cytokine analysis. Results Umbilical artery (UA), descending aorta (DAO), and ductus venosus (DV) pulsatility indices (PI) were significantly higher at each study point in maternal hyperglycemia compared to controls. Placental size, glycogen storages, venous thrombosis formation, and fluid accumulation were increased in maternal hyperglycemia. Epidermal growth factor receptor (Edgfrb), platelet derived growth factor receptor beta polypeptide (Pdgfrb), and tumor necrosis factor receptor superfamily, member 12α (Tnfrsf12α) expressions were decreased. Interleukin (IL) -2 and -4 concentrations were decreased, and IL-1beta levels were increased in maternal hyperglycemia. UA PIs correlated positively with DV PIV, DAO PI, fluid accumulation, and glycogen storages. UA PIs correlated negatively with IL-4, Edgfrb, and Pdgfrb. Discussion In maternal hyperglycemia, placental and fetal hemodynamics were compromised during the last trimester of pregnancy compared to normoglycemic pregnancies. Placental structural, metabolic, and growth related gene expression, and inflammatory marker abnormalities were associated with hemodynamic compromise.

AB - Introduction Human type 1 diabetic pregnancy is associated with placental structural and hemodynamic abnormalities. We hypothesized that in rat fetuses of hyperglycemic dams, placental and fetal blood flow velocity waveforms demonstrate compromised hemodynamics when compared to control fetuses, and these hemodynamic parameters correlate with placental structural abnormalities at near term gestation. Methods Streptozotocin-induced maternal hyperglycemia group comprised 10 dams with 107 fetuses and the control group 20 dams with 219 fetuses. Doppler-ultrasonographic examinations were performed at gestational days 13-14, 16-17, and 19-21. After the last examination, placentas were collected for morphologic, gene expression, and cytokine analysis. Results Umbilical artery (UA), descending aorta (DAO), and ductus venosus (DV) pulsatility indices (PI) were significantly higher at each study point in maternal hyperglycemia compared to controls. Placental size, glycogen storages, venous thrombosis formation, and fluid accumulation were increased in maternal hyperglycemia. Epidermal growth factor receptor (Edgfrb), platelet derived growth factor receptor beta polypeptide (Pdgfrb), and tumor necrosis factor receptor superfamily, member 12α (Tnfrsf12α) expressions were decreased. Interleukin (IL) -2 and -4 concentrations were decreased, and IL-1beta levels were increased in maternal hyperglycemia. UA PIs correlated positively with DV PIV, DAO PI, fluid accumulation, and glycogen storages. UA PIs correlated negatively with IL-4, Edgfrb, and Pdgfrb. Discussion In maternal hyperglycemia, placental and fetal hemodynamics were compromised during the last trimester of pregnancy compared to normoglycemic pregnancies. Placental structural, metabolic, and growth related gene expression, and inflammatory marker abnormalities were associated with hemodynamic compromise.

KW - Animal model

KW - Circulation

KW - Impedance

KW - Maternal hyperglycemia

KW - Placenta

UR - http://www.scopus.com/inward/record.url?scp=84975037746&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84975037746&partnerID=8YFLogxK

U2 - 10.1016/j.placenta.2016.06.002

DO - 10.1016/j.placenta.2016.06.002

M3 - Article

VL - 44

SP - 54

EP - 60

JO - Placenta

JF - Placenta

SN - 0143-4004

ER -