Increased production of tumor necrosis factor-α TNF-α by IUGR human placentae

Gershon Holcberg, Mahmoud Huleihel, Olga Sapir, Miriam Katz, Marina Tsadkin, Boris Furman, Moshe Mazor, Leslie Myatt

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Objective: To evaluate the effect of pathological placental conditions such as intrauterine growth restriction (IUGR) or exposure to angiotensin II (AII) on TNF-α secretion in the vasculature of isolated human placental cotyledons. Study design: Isolated placental cotyledons from 10 normal and four intrauterine growth restricted fetuses were dually perfused. Perfusate samples from the fetal circulation were collected every 30 min during 120 min. TNF-α levels in the fetal-placental perfusate were evaluated using specific commercial ELISA kits. In three additional normal placentae, bolus injections of angiotensin II (10-9 -10-4 mol/l) were given into the fetal-placental circulation and perfusate samples were collected. Statistical significance of difference TNF-α levels between different conditions was determined by analysis of variance (ANOVA) and paired t-test. Results: TNF-α levels were significantly higher in the perfusate of IUGR placentae as compared with normal placentae after 120 min of perfusion (mean 410±121 vs. 39±14 pg/ml, P = 0.005). There was a significant dose-dependent increase in TNF-α levels in the placental perfusate after a bolus injection of AII 66 pg/ml with AII 10-9 mol/l vs. 97 pg/ml with AII 10-5 mol/l (P = 0.004), respectively. Conclusions: Placental pathology related to condition IUGR might induce the secretion of proinflammatory cytokines such as TNF-α, which may enhance the vasoconstriction of the fetal placental vascular bed.

Original languageEnglish (US)
Pages (from-to)69-72
Number of pages4
JournalEuropean Journal of Obstetrics Gynecology and Reproductive Biology
Volume94
Issue number1
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Angiotensin II
Placenta
Tumor Necrosis Factor-alpha
Growth
Cotyledon
Placental Circulation
Injections
Vasoconstriction
Blood Vessels
Analysis of Variance
Fetus
Perfusion
Enzyme-Linked Immunosorbent Assay
Pathology
Cytokines

Keywords

  • Angiotensin II
  • Inflammatory cytokines
  • IUGR
  • Placenta
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Reproductive Medicine

Cite this

Increased production of tumor necrosis factor-α TNF-α by IUGR human placentae. / Holcberg, Gershon; Huleihel, Mahmoud; Sapir, Olga; Katz, Miriam; Tsadkin, Marina; Furman, Boris; Mazor, Moshe; Myatt, Leslie.

In: European Journal of Obstetrics Gynecology and Reproductive Biology, Vol. 94, No. 1, 2001, p. 69-72.

Research output: Contribution to journalArticle

Holcberg, Gershon ; Huleihel, Mahmoud ; Sapir, Olga ; Katz, Miriam ; Tsadkin, Marina ; Furman, Boris ; Mazor, Moshe ; Myatt, Leslie. / Increased production of tumor necrosis factor-α TNF-α by IUGR human placentae. In: European Journal of Obstetrics Gynecology and Reproductive Biology. 2001 ; Vol. 94, No. 1. pp. 69-72.
@article{a1ac85a4dc454ad9bdbc3f6262b539e0,
title = "Increased production of tumor necrosis factor-α TNF-α by IUGR human placentae",
abstract = "Objective: To evaluate the effect of pathological placental conditions such as intrauterine growth restriction (IUGR) or exposure to angiotensin II (AII) on TNF-α secretion in the vasculature of isolated human placental cotyledons. Study design: Isolated placental cotyledons from 10 normal and four intrauterine growth restricted fetuses were dually perfused. Perfusate samples from the fetal circulation were collected every 30 min during 120 min. TNF-α levels in the fetal-placental perfusate were evaluated using specific commercial ELISA kits. In three additional normal placentae, bolus injections of angiotensin II (10-9 -10-4 mol/l) were given into the fetal-placental circulation and perfusate samples were collected. Statistical significance of difference TNF-α levels between different conditions was determined by analysis of variance (ANOVA) and paired t-test. Results: TNF-α levels were significantly higher in the perfusate of IUGR placentae as compared with normal placentae after 120 min of perfusion (mean 410±121 vs. 39±14 pg/ml, P = 0.005). There was a significant dose-dependent increase in TNF-α levels in the placental perfusate after a bolus injection of AII 66 pg/ml with AII 10-9 mol/l vs. 97 pg/ml with AII 10-5 mol/l (P = 0.004), respectively. Conclusions: Placental pathology related to condition IUGR might induce the secretion of proinflammatory cytokines such as TNF-α, which may enhance the vasoconstriction of the fetal placental vascular bed.",
keywords = "Angiotensin II, Inflammatory cytokines, IUGR, Placenta, Tumor necrosis factor",
author = "Gershon Holcberg and Mahmoud Huleihel and Olga Sapir and Miriam Katz and Marina Tsadkin and Boris Furman and Moshe Mazor and Leslie Myatt",
year = "2001",
doi = "10.1016/S0301-2115(00)00321-3",
language = "English (US)",
volume = "94",
pages = "69--72",
journal = "European Journal of Obstetrics and Gynecology and Reproductive Biology",
issn = "0028-2243",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Increased production of tumor necrosis factor-α TNF-α by IUGR human placentae

AU - Holcberg, Gershon

AU - Huleihel, Mahmoud

AU - Sapir, Olga

AU - Katz, Miriam

AU - Tsadkin, Marina

AU - Furman, Boris

AU - Mazor, Moshe

AU - Myatt, Leslie

PY - 2001

Y1 - 2001

N2 - Objective: To evaluate the effect of pathological placental conditions such as intrauterine growth restriction (IUGR) or exposure to angiotensin II (AII) on TNF-α secretion in the vasculature of isolated human placental cotyledons. Study design: Isolated placental cotyledons from 10 normal and four intrauterine growth restricted fetuses were dually perfused. Perfusate samples from the fetal circulation were collected every 30 min during 120 min. TNF-α levels in the fetal-placental perfusate were evaluated using specific commercial ELISA kits. In three additional normal placentae, bolus injections of angiotensin II (10-9 -10-4 mol/l) were given into the fetal-placental circulation and perfusate samples were collected. Statistical significance of difference TNF-α levels between different conditions was determined by analysis of variance (ANOVA) and paired t-test. Results: TNF-α levels were significantly higher in the perfusate of IUGR placentae as compared with normal placentae after 120 min of perfusion (mean 410±121 vs. 39±14 pg/ml, P = 0.005). There was a significant dose-dependent increase in TNF-α levels in the placental perfusate after a bolus injection of AII 66 pg/ml with AII 10-9 mol/l vs. 97 pg/ml with AII 10-5 mol/l (P = 0.004), respectively. Conclusions: Placental pathology related to condition IUGR might induce the secretion of proinflammatory cytokines such as TNF-α, which may enhance the vasoconstriction of the fetal placental vascular bed.

AB - Objective: To evaluate the effect of pathological placental conditions such as intrauterine growth restriction (IUGR) or exposure to angiotensin II (AII) on TNF-α secretion in the vasculature of isolated human placental cotyledons. Study design: Isolated placental cotyledons from 10 normal and four intrauterine growth restricted fetuses were dually perfused. Perfusate samples from the fetal circulation were collected every 30 min during 120 min. TNF-α levels in the fetal-placental perfusate were evaluated using specific commercial ELISA kits. In three additional normal placentae, bolus injections of angiotensin II (10-9 -10-4 mol/l) were given into the fetal-placental circulation and perfusate samples were collected. Statistical significance of difference TNF-α levels between different conditions was determined by analysis of variance (ANOVA) and paired t-test. Results: TNF-α levels were significantly higher in the perfusate of IUGR placentae as compared with normal placentae after 120 min of perfusion (mean 410±121 vs. 39±14 pg/ml, P = 0.005). There was a significant dose-dependent increase in TNF-α levels in the placental perfusate after a bolus injection of AII 66 pg/ml with AII 10-9 mol/l vs. 97 pg/ml with AII 10-5 mol/l (P = 0.004), respectively. Conclusions: Placental pathology related to condition IUGR might induce the secretion of proinflammatory cytokines such as TNF-α, which may enhance the vasoconstriction of the fetal placental vascular bed.

KW - Angiotensin II

KW - Inflammatory cytokines

KW - IUGR

KW - Placenta

KW - Tumor necrosis factor

UR - http://www.scopus.com/inward/record.url?scp=0035190502&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035190502&partnerID=8YFLogxK

U2 - 10.1016/S0301-2115(00)00321-3

DO - 10.1016/S0301-2115(00)00321-3

M3 - Article

C2 - 11134828

AN - SCOPUS:0035190502

VL - 94

SP - 69

EP - 72

JO - European Journal of Obstetrics and Gynecology and Reproductive Biology

JF - European Journal of Obstetrics and Gynecology and Reproductive Biology

SN - 0028-2243

IS - 1

ER -