Vitamin A deficiency during rat pregnancy alters placental TNF-alpha signalling and apoptosis

C Antipatis, C J Ashworth, S C Riley, L Hannah, Nigel Hoggard, R.g. Lea

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Problem: Vitamin A is important for immune function and deficiency is associated with adverse pregnancy outcome, In the rat, vitamin A deficiency reduces both foetal number and neonatal survival. The role of the placenta is uncertain. The effects of maternal vitamin A deficiency on placental cytokines and apoptosis have been investigated.

Method of study: Pregnant rats were fed either control or vitamin A free (VAF) diets (n=4/group) from 8 weeks prior to and throughout pregnancy. Day 20 placentas from viable foetuses were examined for immunoexpression of (a) cytokines: tumour necrosis factor-alpha (TNF-alpha), TNFR1 receptor (p55), leptin and leptin receptor, (b) apoptosis: TdT-mediated dUTP nick end-labelling (TUNEL) positive cells, bax and bcl-2.

Results: Placentas from VAF rats, but not controls, exhibited an infiltrate of neutrophils positive for TNF-alpha and leptin. The number of TNFR1 (p55) and TUNEL positive trophoblast cells was increased specifically in areas of neutrophil infiltration. Trophoblast giant cells in VAF placentas exhibited reduced bax but no change in bcl-2.

Conclusions: Maternal vitamin A deficiency is associated with abnormal placental apoptosis induced by neutrophil derived TNF-alpha acting through the TNFR1 (p55) and/or a change in the bcl-2/bax ratio in the trophoblast giant cells. These changes may underlie the effects of vitamin A deficiency on foetal development.

Original languageEnglish
Pages (from-to)151-158
Number of pages8
JournalAmerican Journal of Reproductive Immunology
Volume47
Issue number3
Publication statusPublished - 1 Mar 2002

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Vitamin A Deficiency
Receptors, Tumor Necrosis Factor, Type I
Vitamin A
Placenta
Trophoblasts
Tumor Necrosis Factor-alpha
Apoptosis
Leptin Receptors
Pregnancy
Giant Cells
Neutrophils
Mothers
Cytokines
Neutrophil Infiltration
Pregnancy Outcome
Fetal Development
Leptin
Fetus
Diet

Keywords

  • Animals
  • Antigens, CD
  • Apoptosis
  • Female
  • Immunohistochemistry
  • Leptin
  • Neutrophils
  • Placenta
  • Pregnancy
  • Pregnancy Complications
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Receptors, Cell Surface
  • Receptors, Leptin
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha
  • Vitamin A Deficiency
  • bcl-2-Associated X Protein

Cite this

Vitamin A deficiency during rat pregnancy alters placental TNF-alpha signalling and apoptosis. / Antipatis, C ; Ashworth, C J ; Riley, S C ; Hannah, L ; Hoggard, Nigel; Lea, R.g.

In: American Journal of Reproductive Immunology, Vol. 47, No. 3, 01.03.2002, p. 151-158.

Research output: Contribution to journalArticle

Antipatis, C, Ashworth, CJ, Riley, SC, Hannah, L, Hoggard, N & Lea, RG 2002, 'Vitamin A deficiency during rat pregnancy alters placental TNF-alpha signalling and apoptosis', American Journal of Reproductive Immunology, vol. 47, no. 3, pp. 151-158.
Antipatis, C ; Ashworth, C J ; Riley, S C ; Hannah, L ; Hoggard, Nigel ; Lea, R.g. / Vitamin A deficiency during rat pregnancy alters placental TNF-alpha signalling and apoptosis. In: American Journal of Reproductive Immunology. 2002 ; Vol. 47, No. 3. pp. 151-158.
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abstract = "Problem: Vitamin A is important for immune function and deficiency is associated with adverse pregnancy outcome, In the rat, vitamin A deficiency reduces both foetal number and neonatal survival. The role of the placenta is uncertain. The effects of maternal vitamin A deficiency on placental cytokines and apoptosis have been investigated.Method of study: Pregnant rats were fed either control or vitamin A free (VAF) diets (n=4/group) from 8 weeks prior to and throughout pregnancy. Day 20 placentas from viable foetuses were examined for immunoexpression of (a) cytokines: tumour necrosis factor-alpha (TNF-alpha), TNFR1 receptor (p55), leptin and leptin receptor, (b) apoptosis: TdT-mediated dUTP nick end-labelling (TUNEL) positive cells, bax and bcl-2.Results: Placentas from VAF rats, but not controls, exhibited an infiltrate of neutrophils positive for TNF-alpha and leptin. The number of TNFR1 (p55) and TUNEL positive trophoblast cells was increased specifically in areas of neutrophil infiltration. Trophoblast giant cells in VAF placentas exhibited reduced bax but no change in bcl-2.Conclusions: Maternal vitamin A deficiency is associated with abnormal placental apoptosis induced by neutrophil derived TNF-alpha acting through the TNFR1 (p55) and/or a change in the bcl-2/bax ratio in the trophoblast giant cells. These changes may underlie the effects of vitamin A deficiency on foetal development.",
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T1 - Vitamin A deficiency during rat pregnancy alters placental TNF-alpha signalling and apoptosis

AU - Antipatis, C

AU - Ashworth, C J

AU - Riley, S C

AU - Hannah, L

AU - Hoggard, Nigel

AU - Lea, R.g.

PY - 2002/3/1

Y1 - 2002/3/1

N2 - Problem: Vitamin A is important for immune function and deficiency is associated with adverse pregnancy outcome, In the rat, vitamin A deficiency reduces both foetal number and neonatal survival. The role of the placenta is uncertain. The effects of maternal vitamin A deficiency on placental cytokines and apoptosis have been investigated.Method of study: Pregnant rats were fed either control or vitamin A free (VAF) diets (n=4/group) from 8 weeks prior to and throughout pregnancy. Day 20 placentas from viable foetuses were examined for immunoexpression of (a) cytokines: tumour necrosis factor-alpha (TNF-alpha), TNFR1 receptor (p55), leptin and leptin receptor, (b) apoptosis: TdT-mediated dUTP nick end-labelling (TUNEL) positive cells, bax and bcl-2.Results: Placentas from VAF rats, but not controls, exhibited an infiltrate of neutrophils positive for TNF-alpha and leptin. The number of TNFR1 (p55) and TUNEL positive trophoblast cells was increased specifically in areas of neutrophil infiltration. Trophoblast giant cells in VAF placentas exhibited reduced bax but no change in bcl-2.Conclusions: Maternal vitamin A deficiency is associated with abnormal placental apoptosis induced by neutrophil derived TNF-alpha acting through the TNFR1 (p55) and/or a change in the bcl-2/bax ratio in the trophoblast giant cells. These changes may underlie the effects of vitamin A deficiency on foetal development.

AB - Problem: Vitamin A is important for immune function and deficiency is associated with adverse pregnancy outcome, In the rat, vitamin A deficiency reduces both foetal number and neonatal survival. The role of the placenta is uncertain. The effects of maternal vitamin A deficiency on placental cytokines and apoptosis have been investigated.Method of study: Pregnant rats were fed either control or vitamin A free (VAF) diets (n=4/group) from 8 weeks prior to and throughout pregnancy. Day 20 placentas from viable foetuses were examined for immunoexpression of (a) cytokines: tumour necrosis factor-alpha (TNF-alpha), TNFR1 receptor (p55), leptin and leptin receptor, (b) apoptosis: TdT-mediated dUTP nick end-labelling (TUNEL) positive cells, bax and bcl-2.Results: Placentas from VAF rats, but not controls, exhibited an infiltrate of neutrophils positive for TNF-alpha and leptin. The number of TNFR1 (p55) and TUNEL positive trophoblast cells was increased specifically in areas of neutrophil infiltration. Trophoblast giant cells in VAF placentas exhibited reduced bax but no change in bcl-2.Conclusions: Maternal vitamin A deficiency is associated with abnormal placental apoptosis induced by neutrophil derived TNF-alpha acting through the TNFR1 (p55) and/or a change in the bcl-2/bax ratio in the trophoblast giant cells. These changes may underlie the effects of vitamin A deficiency on foetal development.

KW - Animals

KW - Antigens, CD

KW - Apoptosis

KW - Female

KW - Immunohistochemistry

KW - Leptin

KW - Neutrophils

KW - Placenta

KW - Pregnancy

KW - Pregnancy Complications

KW - Proto-Oncogene Proteins

KW - Proto-Oncogene Proteins c-bcl-2

KW - Rats

KW - Receptors, Cell Surface

KW - Receptors, Leptin

KW - Receptors, Tumor Necrosis Factor

KW - Receptors, Tumor Necrosis Factor, Type I

KW - Tumor Necrosis Factor-alpha

KW - Vitamin A Deficiency

KW - bcl-2-Associated X Protein

M3 - Article

C2 - 12069200

VL - 47

SP - 151

EP - 158

JO - American Journal of Reproductive Immunology

JF - American Journal of Reproductive Immunology

SN - 8755-8920

IS - 3

ER -