ArticlePhysiological genomics2014
Transcriptomics of the fetal hypothalamic response to brachiocephalic occlusion and estradiol treatment.
Article in Physiological genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Gestational Hypoxia and Blood-Brain Barrier Permeability: Early Origins of Cerebrovascular Dysfunction Induced by Epigenetic Mechanisms.Frontiers in physiology · 2021Review
- Current paradigms and new perspectives on fetal hypoxia: implications for fetal brain development in late gestation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Review
- Effects of ketamine on the fetal transcriptomic response to umbilical cord occlusion: comparison with hypoxic hypoxia in the cerebral cortex.The Journal of physiology · 2018Article
- A transcriptomics model of estrogen action in the ovine fetal hypothalamus: evidence for estrogenic effects of ICI 182,780.Physiological reports · 2018Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Hypothalamic transcriptomic alterations in male and female California mice (Physiological reports · 2017Article
- Ketamine decreases inflammatory and immune pathways after transient hypoxia in late gestation fetal cerebral cortex.Physiological reports · 2016Article
- Ketamine suppresses hypoxia-induced inflammatory responses in the late-gestation ovine fetal kidney cortex.The Journal of physiology · 2016Article
- Transcriptomics Modeling of the Late-Gestation Fetal Pituitary Response to Transient Hypoxia.PloS one · 2016Article
- A question of cytokine signaling in the fetus.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Interleukin-1β transfer across the blood-brain barrier in the ovine fetus.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Estradiol (E2) is a well-known modulator of fetal neuroendocrine activity and has been proposed as a critical endocrine signal readying the fetus for birth and postnatal life. To investigate the modulatory role of E2 on fetal stress responsiveness and the response of the fetal brain to asphyxic stress, we subjected chronically catheterized fetal sheep to a transient (10 min) brachiocephalic artery occlusion (BCO) or sham occlusion. Half of the fetuses received subcutaneous pellets that increased plasma E2 concentrations within the physiological range. Hypothalamic mRNA was analyzed using the Agilent 8x15k ovine array (019921), processed and annotated as previously reported by our laboratory. Analysis of the data by ANOVA revealed that E2 differentially regulated (DR) 561 genes, and BCO DR 894 genes compared with control and E2+BCO DR 1,153 genes compared with BCO alone (all P < 0.05). E2 upregulated epigenetic pathways and downregulated local steroid biosynthesis but did not significantly involve genes known to directly respond to the estrogen receptor. Brachiocephalic occlusion upregulated kinase pathways as well as genes associated with lymphocyte infiltration into the brain and downregulated neuropeptide synthesis. E2 upregulated immune- and apoptosis-related pathways after BCO and reduced kinase and epigenetic pathway responses to the BCO. Responses to BCO are different from responses to hypoxic hypoxia suggesting that mechanisms of responses to these two forms of brain hypoxia are distinct. We conclude that cerebral ischemia caused by BCO might stimulate lymphocyte infiltration into the brain and that this response appears to be modified by estradiol.
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