Background: A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery ligation. Methods: Sprague-Dawley rats underwent uterine artery ligation at day 19 of gestation. Offspring were sacrificed at 5, 20 and 40 days post-partum. Follicles were counted and classified in hematoxylin-eosin stained sections. Gene expression of 90 genes was analyzed by TaqMan® Low Density Array. Results: A significantly lower number of total and primordial follicles was detected in 20 days post-partum intrauterine growth restricted animals. Follicle density was not different at 40 days post-partum, suggesting that compensatory mechanisms occurred during the pre-pubertal window. Uterine artery ligation modified the expression of 24 genes involved in different cellular functions, among which proliferation, apoptosis and metabolism. Conclusion: Ovarian follicle pool was affected by fetal hypoxia in early life, but this effect did not persist in puberty. Genes involved in cellular processes were affected at all ages, potentially implying long-term genetic alterations. Further analyses are needed to elucidate later effects of fetal hypoxia on ovarian function and fertility.

Pampanini, V., Jahnukainen, K., Sahlin, L., Germani, D., Puglianiello, A., Cianfarani, S., et al. (2019). Impact of uteroplacental insufficiency on ovarian follicular pool in the rat. REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY, 17(1), 10 [10.1186/s12958-019-0453-3].

Impact of uteroplacental insufficiency on ovarian follicular pool in the rat

Pampanini V.;Germani D.;Puglianiello A.;Cianfarani S.;
2019-01-01

Abstract

Background: A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery ligation. Methods: Sprague-Dawley rats underwent uterine artery ligation at day 19 of gestation. Offspring were sacrificed at 5, 20 and 40 days post-partum. Follicles were counted and classified in hematoxylin-eosin stained sections. Gene expression of 90 genes was analyzed by TaqMan® Low Density Array. Results: A significantly lower number of total and primordial follicles was detected in 20 days post-partum intrauterine growth restricted animals. Follicle density was not different at 40 days post-partum, suggesting that compensatory mechanisms occurred during the pre-pubertal window. Uterine artery ligation modified the expression of 24 genes involved in different cellular functions, among which proliferation, apoptosis and metabolism. Conclusion: Ovarian follicle pool was affected by fetal hypoxia in early life, but this effect did not persist in puberty. Genes involved in cellular processes were affected at all ages, potentially implying long-term genetic alterations. Further analyses are needed to elucidate later effects of fetal hypoxia on ovarian function and fertility.
2019
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/38 - PEDIATRIA GENERALE E SPECIALISTICA
English
Developmental origins of health and disease; Follicle reserve; Intrauterine growth restriction; Ovary; Animals; Body Weight; Female; Fetal Growth Retardation; Gene Regulatory Networks; Hypoxia; Ligation; Organ Size; Ovarian Follicle; Pregnancy; Rats, Sprague-Dawley; Uterine Artery; Gene Expression Profiling; Gene Expression Regulation, Developmental
http://www.rbej.com/home/
Pampanini, V., Jahnukainen, K., Sahlin, L., Germani, D., Puglianiello, A., Cianfarani, S., et al. (2019). Impact of uteroplacental insufficiency on ovarian follicular pool in the rat. REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY, 17(1), 10 [10.1186/s12958-019-0453-3].
Pampanini, V; Jahnukainen, K; Sahlin, L; Germani, D; Puglianiello, A; Cianfarani, S; Soder, O
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/232138
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