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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...

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Related Experiment Video

Updated: Nov 12, 2025

Quantification of Vascular Parameters in Whole Mount Retinas of Mice with Non-Proliferative and Proliferative Retinopathies

Quantification of Vascular Parameters in Whole Mount Retinas of Mice with Non-Proliferative and Proliferative Retinopathies

Published on: March 12, 2022

Retinal hypoxia and angiogenesis with methamphetamine.

Minsup Lee¹, Wendy Leskova¹, Randa S Eshaq¹

¹Department of Molecular & Cellular Physiology, Louisiana State University Health Shreveport, Shreveport, LA, 71103, USA.

Experimental Eye Research

|March 19, 2021

Summary

This summary is machine-generated.

Methamphetamine (METH) abuse can cause eye damage. This study shows METH induces retinal hypoxia, increasing blood vessel growth (angiogenesis) by activating hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF).

Keywords:

Angiogenesis HIF-1α Hypoxia Methamphetamine VEGF

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Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model

Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model

Published on: April 2, 2021

Area of Science:

Ophthalmology
Toxicology
Vascular Biology

Background:

Methamphetamine (METH) abuse is linked to severe ocular complications, including central retinal artery occlusion and retinopathy.
Retinal neovascularization, a condition where new blood vessels grow abnormally, has been observed in METH abusers.

Purpose of the Study:

To investigate if METH administration induces retinal neovascularization in a mouse model.
To determine if METH-induced neovascularization is associated with increased retinal hypoxia, hypoxia-inducible factor 1α (HIF-1α), and vascular endothelial growth factor (VEGF).

Main Methods:

Mice were administered METH or saline (vehicle control) via intraperitoneal injection over 26 days.
Retinal vascularity was assessed using in vivo imaging and flat-mounted retinas stained with Griffonia simplicifolia lectin I.
Retinal hypoxia, HIF-1α, and VEGFa protein levels were measured using pimonidazole adducts and immunoblotting.

Main Results:

METH administration significantly increased retinal vascularity and the number of arterioles by Day 26.
Retinal VEGFa protein levels increased on Days 12 and 26 in METH-treated mice.
Increased retinal hypoxia and HIF-1α protein expression were observed on Days 12 and 26.

Conclusions:

Methamphetamine administration induces retinal hypoxia, HIF-1α activation, and VEGFa upregulation.
These molecular changes promote angiogenesis in the retina.
The findings suggest a mechanism by which METH abuse can lead to sight-threatening ocular neovascularization.