Maternal hypoxia as a model for intrauterine growth retardation: Effects on insulin-like growth factors and their binding proteins

Paivi J. Tapanainen, Peter Bang, Kristin Wilson, Terry G. Unterman, Hendrik J. Vreman, Ronald (Ron) Rosenfeld

Research output: Contribution to journalArticle

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Abstract

Evidence suggests that IGF and their binding proteins play a role in fetal growth, but more knowledge concerning their regulation is essential. We examined the expression of IGF and their binding proteins in experimental intrauterine growth-retarded (IUGR) rat fetuses of hypoxic dams (1314% oxygen, d 14-21 of gestation). The mean body weight of the fetuses (d 21 of gestation, n = 72) of the six hypoxic dams was 24% lower (p <0.0001) than the mean weight of the fetuses of six control dams (n = 82). Wet liver weights demonstrated a 20% decrease (p <0.0001) and placentas a 10% decrease (p <0.01) compared with control fetuses. The mean serum concentrations of immunoreactive 1GF-I in both groups were low but did not differ significantly. The mean serum concentrations of immunoreactive IGF-II, however, were higher in IUGR fetuses. As assessed by Northern blot analysis, there was a 4-fold increase in insulin-like growth factor binding protein-1 (IGFBP-1) mRNA expression in the livers of the IUGR fetuses compared with controls. IGFBP-2 mRNA expression was 6-fold increased in IUGR fetal livers. No difference was found in IGFBP-4 mRNA. An increase in IGFBP-1, -2, and -4 concentrations could be seen by Western ligand blotting in the serum of growth-retarded fetuses compared with control fetuses. This finding was verified by immunoprecipitation with specific antibodies, which demonstrated increases in IGFBP-1 and IGFBP-2. Our results validate the use of maternal hypoxia as an experimental model of intrauterine growth retardation and indicate that increased IGFBP-1 and -2 expression may be of importance in the etiology of fetal growth retardation caused by maternal hypoxia.

Original languageEnglish (US)
Pages (from-to)152-158
Number of pages7
JournalPediatric Research
Volume36
Issue number2
StatePublished - 1994
Externally publishedYes

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Insulin-Like Growth Factor Binding Proteins
Fetal Growth Retardation
Fetus
Mothers
Insulin-Like Growth Factor Binding Protein 2
Insulin-Like Growth Factor Binding Protein 1
Growth
Fetal Development
Messenger RNA
Liver
Serum
Insulin-Like Growth Factor Binding Protein 4
Weights and Measures
Pregnancy
Insulin-Like Growth Factor II
Hypoxia
Immunoprecipitation
Northern Blotting
Placenta
Theoretical Models

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Tapanainen, P. J., Bang, P., Wilson, K., Unterman, T. G., Vreman, H. J., & Rosenfeld, R. R. (1994). Maternal hypoxia as a model for intrauterine growth retardation: Effects on insulin-like growth factors and their binding proteins. Pediatric Research, 36(2), 152-158.

Maternal hypoxia as a model for intrauterine growth retardation : Effects on insulin-like growth factors and their binding proteins. / Tapanainen, Paivi J.; Bang, Peter; Wilson, Kristin; Unterman, Terry G.; Vreman, Hendrik J.; Rosenfeld, Ronald (Ron).

In: Pediatric Research, Vol. 36, No. 2, 1994, p. 152-158.

Research output: Contribution to journalArticle

Tapanainen, PJ, Bang, P, Wilson, K, Unterman, TG, Vreman, HJ & Rosenfeld, RR 1994, 'Maternal hypoxia as a model for intrauterine growth retardation: Effects on insulin-like growth factors and their binding proteins', Pediatric Research, vol. 36, no. 2, pp. 152-158.
Tapanainen, Paivi J. ; Bang, Peter ; Wilson, Kristin ; Unterman, Terry G. ; Vreman, Hendrik J. ; Rosenfeld, Ronald (Ron). / Maternal hypoxia as a model for intrauterine growth retardation : Effects on insulin-like growth factors and their binding proteins. In: Pediatric Research. 1994 ; Vol. 36, No. 2. pp. 152-158.
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AB - Evidence suggests that IGF and their binding proteins play a role in fetal growth, but more knowledge concerning their regulation is essential. We examined the expression of IGF and their binding proteins in experimental intrauterine growth-retarded (IUGR) rat fetuses of hypoxic dams (1314% oxygen, d 14-21 of gestation). The mean body weight of the fetuses (d 21 of gestation, n = 72) of the six hypoxic dams was 24% lower (p <0.0001) than the mean weight of the fetuses of six control dams (n = 82). Wet liver weights demonstrated a 20% decrease (p <0.0001) and placentas a 10% decrease (p <0.01) compared with control fetuses. The mean serum concentrations of immunoreactive 1GF-I in both groups were low but did not differ significantly. The mean serum concentrations of immunoreactive IGF-II, however, were higher in IUGR fetuses. As assessed by Northern blot analysis, there was a 4-fold increase in insulin-like growth factor binding protein-1 (IGFBP-1) mRNA expression in the livers of the IUGR fetuses compared with controls. IGFBP-2 mRNA expression was 6-fold increased in IUGR fetal livers. No difference was found in IGFBP-4 mRNA. An increase in IGFBP-1, -2, and -4 concentrations could be seen by Western ligand blotting in the serum of growth-retarded fetuses compared with control fetuses. This finding was verified by immunoprecipitation with specific antibodies, which demonstrated increases in IGFBP-1 and IGFBP-2. Our results validate the use of maternal hypoxia as an experimental model of intrauterine growth retardation and indicate that increased IGFBP-1 and -2 expression may be of importance in the etiology of fetal growth retardation caused by maternal hypoxia.

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