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Related Concept Videos

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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Hypoxia01:23

Hypoxia

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Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

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Paracrine Signaling

Paracrine signaling allows cells to communicate with their immediate neighbors via secretion of signaling molecules. Such a signal can only trigger a response in nearby target cells because the signal molecules degrade quickly or are inactivated if not taken up. Prominent examples of paracrine signaling include nitric oxide signaling in blood vessels, synaptic signaling of neurons, the blood clotting system, tissue repair/wound healing, and local allergic skin reactions. Nitric oxide as a...
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Oxygen Transport in the Blood

Hemoglobin (Hb) is a crucial molecule in the human body, consisting of four polypeptide chains, each bound to an iron-containing heme group. This unique structure enables hemoglobin to bind to oxygen, with each molecule capable of combining with four molecules of oxygen, leading to rapid and reversible oxygen loading. When fully loaded with oxygen, it is called oxyhemoglobin, while hemoglobin that has released oxygen is called reduced hemoglobin or deoxyhemoglobin. As hemoglobin binds oxygen,...

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Induction and Testing of Hypoxia in Cell Culture
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Published on: August 12, 2011

Endothelial cell COX-2 expression and activity in hypoxia.

Rebecca J Cook-Johnson1, Maryanne Demasi, Leslie G Cleland

  • 1Rheumatology Unit, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia.

Biochimica Et Biophysica Acta
|October 19, 2006
PubMed
Summary

Hypoxia increases prostacyclin (PGI(2)) synthesis in endothelial cells, a process dependent on cyclooxygenase-2 (COX-2) upregulation. Hypoxia-inducible factors (HIFs) mediate this COX-2 response, highlighting a protective cardiovascular mechanism.

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Last Updated: Jul 19, 2026

Induction and Testing of Hypoxia in Cell Culture
07:01

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Published on: August 12, 2011

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

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Published on: August 2, 2018

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08:32

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair

Published on: March 22, 2024

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Endothelial Cell Function

Background:

  • Cyclooxygenase-2 (COX-2) plays a protective role in the cardiovascular system.
  • Endothelial cells synthesize eicosanoids, crucial signaling molecules.
  • Hypoxia significantly impacts cellular function and molecular regulation.

Purpose of the Study:

  • To investigate the role of COX-2 in endothelial cell eicosanoid synthesis during hypoxia.
  • To elucidate the molecular mechanisms regulating COX-2 expression in response to hypoxia.
  • To examine the involvement of Hypoxia-Inducible Factors (HIFs) in this process.

Main Methods:

  • Exposure of human umbilical vein endothelial cells (HUVEC) to hypoxia.
  • Measurement of COX-2, prostacyclin (PGI(2)), and thromboxane (TXA(2)) synthesis.
  • Analysis of COX-2 promoter constructs and transcription factor binding sites (HIFs, NF-kappaB).
  • Use of HIF expression vectors and electrophoretic mobility shift assays (EMSA).

Main Results:

  • Hypoxia increased PGI(2) synthesis, but not TXA(2) synthesis.
  • PGI(2) production was COX-2 dependent and upregulated by hypoxia.
  • HIFs, not NF-kappaB, were implicated in hypoxia-induced COX-2 upregulation.
  • HIFs bound to the COX-2 promoter and increased COX-2 expression.

Conclusions:

  • Endothelial cells increase anti-thrombotic PGI(2) production under hypoxia.
  • This response is mediated by COX-2 upregulation.
  • Hypoxia-inducible factors (HIFs) are key regulators of COX-2 in hypoxic endothelial cells.
  • This HIF-mediated pathway represents an important endogenous protective mechanism.