Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hypoxia01:23

Hypoxia

Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...
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...
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Streamlining Global Germplasm Exchange: Integrating Scientific Rigor and Common Sense to Exclude Phantom Agents from Regulation.

Plant disease·2025
Same author

The Detection and Variation of Strawberry mottle virus.

Plant disease·2019
Same author

The effect of diazepam on isoflurane-fentanyl minimum alveolar concentration (MAC) in the dog.

Veterinary anaesthesia and analgesia·2017
Same author

The use of pulsed electromagnetic field (PEMF) therapy to provide post-operative analgesia in the dog.

Veterinary anaesthesia and analgesia·2017
Same author

Evaluation of xylazine and ketamine for maintenance of anesthesia in horses.

Veterinary anaesthesia and analgesia·2017
Same author

Cardiopulmonary measurements in six horses with naturally-acquired colic (acute abdominal crisis).

Veterinary anaesthesia and analgesia·2017

Related Experiment Video

Updated: Jul 5, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
09:17

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Published on: August 2, 2018

Dexamethasone impairs hypoxia-inducible factor-1 function.

A E Wagner1, G Huck, D P Stiehl

  • 1Institute of Physiology, University of Luebeck, Ratzeburger Allee 160, D-23538 Luebeck, Germany.

Biochemical and Biophysical Research Communications
|May 27, 2008
PubMed
Summary

Glucocorticoids inhibit hypoxia-inducible factor-1 (HIF-1) dependent gene expression by reducing nuclear HIF-1 levels and DNA-binding. This finding may explain impaired wound healing in patients treated with glucocorticoids.

More Related Videos

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice
09:13

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice

Published on: July 11, 2025

Induction and Testing of Hypoxia in Cell Culture
07:01

Induction and Testing of Hypoxia in Cell Culture

Published on: August 12, 2011

Related Experiment Videos

Last Updated: Jul 5, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
09:17

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Published on: August 2, 2018

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice
09:13

Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice

Published on: July 11, 2025

Induction and Testing of Hypoxia in Cell Culture
07:01

Induction and Testing of Hypoxia in Cell Culture

Published on: August 12, 2011

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Pharmacology

Background:

  • Hypoxia-inducible factor-1 (HIF-1) regulates cellular adaptation to low oxygen, inflammation, and wound healing.
  • Glucocorticoids (GC) are potent anti-inflammatory drugs.
  • The interaction between GC and HIF-1 signaling is not fully understood.

Purpose of the Study:

  • To investigate the effect of glucocorticoids on HIF-1 function and downstream gene expression.
  • To determine the role of the glucocorticoid receptor (GR) in mediating these effects.

Main Methods:

  • Utilized human hepatoma cell lines (HepG2 with GR, Hep3B lacking GR) as model systems.
  • Treated cells with dexamethasone (DEX) under normoxic and hypoxic conditions.
  • Assessed HIF-1alpha protein levels, nuclear translocation, DNA-binding activity, and reporter gene activity (luciferase).
  • Measured expression of HIF-1 target gene VEGF.

Main Results:

  • Dexamethasone increased cytosolic HIF-1alpha but decreased nuclear HIF-1alpha and DNA-binding in GR-positive HepG2 cells.
  • DEX suppressed hypoxia-induced reporter gene activity and VEGF expression in HepG2 cells.
  • These inhibitory effects were absent in GR-deficient Hep3B and HRB5 cells.
  • Restoring GR expression in HRB5 cells re-established sensitivity to DEX.

Conclusions:

  • Glucocorticoids inhibit HIF-1 dependent gene expression through a GR-mediated mechanism.
  • This inhibition involves reduced nuclear translocation and DNA-binding of HIF-1.
  • The findings highlight a potential mechanism for impaired wound healing observed in patients receiving glucocorticoid therapy.