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Condition: Hypertension
Drug: Estradiol

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Total 4 results found since Jan 2013.

17β-estradiol and estrogen receptor α protect right ventricular function in pulmonary hypertension via BMPR2 and apelin
Women with pulmonary arterial hypertension (PAH) exhibit better right ventricular (RV) function and survival than men; however, the underlying mechanisms are unknown. We hypothesized that 17β-estradiol (E2), through estrogen receptor α (ER-α), attenuates PAH-induced RV failure (RVF) by upregulating the procontractile and prosurvival peptide apelin via a BMPR2-dependent mechanism. We found that ER-α and apelin expression were decreased in RV homogenates from patients with RVF and from rats with maladaptive (but not adaptive) RV remodeling. RV cardiomyocyte apelin abundance increased in vivo or in vitro after treatment w...
Source: Journal of Clinical Investigation - March 15, 2021 Category: Biomedical Science Authors: Andrea L. Frump, Marjorie Albrecht, Bakhtiyor Yakubov, Sandra Breuils-Bonnet, Valérie Nadeau, Eve Tremblay, Francois Potus, Junichi Omura, Todd Cook, Amanda Fisher, Brooke Rodriguez, R. Dale Brown, Kurt R. Stenmark, C. Dustin Rubinstein, Kathy Krentz, Di Source Type: research

Neonatal cardiomyocyte hypertrophy induced by endothelin-1 is blocked by estradiol acting on GPER.
In conclusion, E2 plays a key role in antagonizing ET-1-induced hypertrophy in cultured neonatal cardiomyocytes through GPER signaling by mechanism involving activation of PDK1 pathway, which would prevent the increase of ERK1/2 activity and consequently the development of hypertrophy. PMID: 29167148 [PubMed - as supplied by publisher]
Source: Am J Physiol Cell Ph... - November 22, 2017 Category: Cytology Authors: Goncalves GK, Scalzo S, Alves AP, Agero U, Guatimosim S, Reis AM Tags: Am J Physiol Cell Physiol Source Type: research

Abstract P098: G-protein Coupled Estrogen Receptor Stimulates Capillary Formation by Human Umbilical Vein Endothelial Cells via ALK1-SMAD 1/5/8 Pathway Activation Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception
Estradiol (E2) induces vascular repair by promoting endothelial growth and capillary formation. Based on our previous findings that the capillary stimulating effects of E2 are mimicked by its non-permeable analog, BSA-tagged E2, we hypothesize that the stimulatory effects are potentially mediated via the newly discovered membrane bound G-protein coupled estrogen receptor (GPER). To investigate this, we assessed capillary formation by endothelial cells in response to E2, and GPER agonist (G1)and antagonist (G15) in a 2-D matrigel based assay. Capillary formation was assessed microscopically by quantifying junction/sprout fo...
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Unterleutner, E., Rigassi, L., Barchiesi, F., Imthurn, B., Dubey, R. K. Tags: Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception Source Type: research

Title: Genistein Disrupts Glucocorticoid Receptor Signaling in Human Uterine Endometrial Ishikawa Cells
Conclusions: Using Ishikawa cells, we observed that exposure to genistein resulted in distinct changes in gene expression and unique differences in the GR transcriptome. Citation: Whirledge S, Senbanjo LT, Cidlowski JA. 2015. Genistein disrupts glucocorticoid receptor signaling in human uterine endometrial Ishikawa cells. Environ Health Perspect 123:80–87; http://dx.doi.org/10.1289/ehp.1408437 Address correspondence to J.A. Cidlowski, NIH/NIEHS, MD F3-07, P.O. Box 12233, Research Triangle Park, NC 27709 USA. Telephone: (919) 541-1564. E-mail: cidlows1@niehs.nih.gov We thank X. Xu (Integrative Bioinformatic...
Source: EHP Research - December 31, 2014 Category: Environmental Health Authors: Web Admin Tags: Research Article January 2015 Source Type: research