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Related Concept Videos

Internal Receptors01:31

Internal Receptors

Many cellular signals are hydrophilic and therefore cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind to internal, or intracellular, receptors that reside within the cell. Many mammalian steroid hormones use this mechanism of cell signaling, as does nitric oxide (NO) gas.
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Types of Receptors: Internal Receptors01:07

Types of Receptors: Internal Receptors

Many cellular signals are hydrophilic and cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind intracellular receptors that reside within the cell cytoplasm or nucleus. Many mammalian steroid hormones and nitric oxide (NO) gas use this cell signaling mechanism.
Similar to membrane-bound receptors, the binding of a ligand to the intracellular receptor of causes a conformational change in the...
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
Target Cell Response to Hormones01:22

Target Cell Response to Hormones

Hormones intricately bind to receptors on the surface or within target cells, initiating a cascade of cellular responses.
Notably, the cellular response can be regulated by altering the number of receptors expressed in the cell. For example, prolonged exposure to elevated hormone levels results in a gradual decline or down-regulation in the number of receptors for that specific hormone on the cell surface. Conversely, in response to low hormone levels, cells may use up-regulation, producing an...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...

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Related Experiment Video

Updated: Jul 10, 2026

Imaging of Estrogen Receptor-α in Rat Pial Arterioles using a Digital Immunofluorescent Microscope
07:42

Imaging of Estrogen Receptor-α in Rat Pial Arterioles using a Digital Immunofluorescent Microscope

Published on: November 29, 2011

Estrogen causes dynamic alterations in endothelial estrogen receptor expression.

Christopher E Ihionkhan1, Ken L Chambliss, Linda L Gibson

  • 1Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75390-9063, USA.

Circulation Research
|November 2, 2002
PubMed
Summary

Estrogen (E2) upregulates estrogen receptor (ER)alpha in endothelial cells with prolonged exposure, while ERbeta expression decreases. These changes in ERalpha and ERbeta may alter estrogen

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Last Updated: Jul 10, 2026

Imaging of Estrogen Receptor-α in Rat Pial Arterioles using a Digital Immunofluorescent Microscope
07:42

Imaging of Estrogen Receptor-α in Rat Pial Arterioles using a Digital Immunofluorescent Microscope

Published on: November 29, 2011

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
10:36

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer

Published on: March 17, 2016

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
06:18

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

Published on: August 13, 2019

Area of Science:

  • Endocrinology
  • Vascular Biology
  • Molecular Biology

Background:

  • Estrogen receptor (ER)alpha plays a key role in mediating estrogen's vascular endothelium effects.
  • Understanding how estrogen influences ER expression in endothelial cells is crucial for vascular health.

Purpose of the Study:

  • To investigate the impact of estrogen on endothelial estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) expression.
  • To elucidate the molecular mechanisms underlying estrogen-induced changes in ER expression in endothelial cells.

Main Methods:

  • Cultured ovine endothelial cells were treated with 17beta-estradiol (E2) at physiological concentrations.
  • ERalpha and ERbeta protein and gene expression were analyzed using Western blotting and RT-PCR.
  • ERalpha gene promoter activity was assessed using luciferase reporter assays.
  • Pharmacological inhibitors and antagonists were employed to dissect signaling pathways.

Main Results:

  • Long-term E2 exposure (≥6 hours) upregulated ERalpha protein and gene transcription in endothelial cells.
  • Short-term E2 exposure (2 hours) initially downregulated ERalpha.
  • ERbeta expression was consistently downregulated by E2.
  • Both ERalpha and ERbeta mediated E2-induced ERalpha gene transcription.

Conclusions:

  • Prolonged estrogen exposure upregulates ERalpha expression in endothelial cells via transcriptional mechanisms involving both ERalpha and ERbeta.
  • Estrogen downregulates ERbeta expression in the endothelium.
  • Modulation of ERalpha and ERbeta levels by estrogen may influence its vascular effects.