ArticleBiology of reproduction2015
Estrogen Regulates Angiotensin II Receptor Expression Patterns and Protects the Heart from Ischemic Injury in Female Rats.
Article in Biology of reproduction, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Sex differences in the sensitization of prenatally programmed hypertension.Frontiers in physiology · 2025Review
- The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease.Frontiers in pharmacology · 2023Review
- Estrogen normalizes maternal HFD-induced vascular dysfunction in offspring by regulating ATR.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Article
- Prenatal Hypoxia Affects Foetal Cardiovascular Regulatory Mechanisms in a Sex- and Circadian-Dependent Manner: A Review.International journal of molecular sciences · 2022Review
- Role of Estrogen Receptor-Positive/Negative Ratios in Regulating Breast Cancer.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Neurodegenerative Disease: Roles for Sex, Hormones, and Oxidative Stress.Endocrinology · 2021Review
- Considering Sex as a Biological Variable in Basic and Clinical Studies: An Endocrine Society Scientific Statement.Endocrine reviews · 2021Article
- Estrogen Receptors: Therapeutic Perspectives for the Treatment of Cardiac Dysfunction after Myocardial Infarction.International journal of molecular sciences · 2021Review
- The counter regulatory axis of the renin angiotensin system in the brain and ischaemic stroke: Insight from preclinical stroke studies and therapeutic potential.Cellular signalling · 2020Review
- Involvement of angiotensin II receptor type 1/NF-κB signaling in the development of endometriosis.Experimental and therapeutic medicine · 2020Article
- Effects of Estrogen in Gender-dependent Fetal Programming of Adult Cardiovascular Dysfunction.Current vascular pharmacology · 2019Review
- Estrogen Contributions to Microvascular Dysfunction Evolving to Heart Failure With Preserved Ejection Fraction.Frontiers in endocrinology · 2019Review
- Long-term exposure to high altitude hypoxia during pregnancy increases fetal heart susceptibility to ischemia/reperfusion injury and cardiac dysfunction.International journal of cardiology · 2019Article
- The detrimental effects of glucocorticoids exposure during pregnancy on offspring's cardiac functions mediated by hypermethylation of bone morphogenetic protein-4.Cell death & disease · 2018Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- MicroRNA-210 suppresses glucocorticoid receptor expression in response to hypoxia in fetal rat cardiomyocytes.Oncotarget · 2017Article
- Sex-specific associations between cerebrovascular blood pressure autoregulation and cardiopulmonary injury in neonatal encephalopathy and therapeutic hypothermia.Pediatric research · 2017Observational
- Effects of Estradiol on the Paracrine Regulator Expression ofTissue engineering and regenerative medicine · 2017Article
- Breaking the Cycle: Estrous Variation Does Not Require Increased Sample Size in the Study of Female Rats.Hypertension (Dallas, Tex. : 1979) · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have shown that female offspring are resistant to fetal stress-induced programming of ischemic-sensitive phenotype in the heart; however, the mechanisms responsible remain unclear. The present study tested the hypothesis that estrogen plays a role in protecting females in fetal programming of increased heart vulnerability. Pregnant rats were divided into normoxic and hypoxic (10.5% O2 from Day 15 to 21 of gestation) groups. Ovariectomy (OVX) and estrogen (E2) replacement were performed in 8-wk-old female offspring. Hearts of 4-mo-old females were subjected to ischemia and reperfusion injury in a Langendorff preparation. OVX significantly decreased postischemic recovery of left ventricular function and increased myocardial infarction, and no difference was observed between normoxic and hypoxic groups. The effect of OVX was rescued by E2 replacement. OVX decreased the binding of glucocorticoid receptor (GR) to glucocorticoid response elements at angiotensin II type 1 (Agtr1) and type 2 (Agtr2) receptor promoters, resulting in a decrease in Agtr1 and an increase in Agtr2 in the heart. Additionally, OVX decreased estrogen receptor (ER) expression in the heart and inhibited ER/GR interaction in binding to glucocorticoid response elements at the promoters. Consistent with the changes in Agtrs, OVX significantly decreased Prkce abundance in the heart. These OVX-induced changes were abrogated by E2 replacement. The results indicate that estrogen is not directly responsible for the sex dimorphism in fetal programming of heart ischemic vulnerability but suggest a novel mechanism of estrogen in regulating cardiac Agtr1/Agtr2 expression patterns and protecting female hearts against ischemia and reperfusion injury.
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