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

You might also read

Related Articles

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

Sort by
Same author

Infiltrating monocytes augment alternative complement activation and exacerbate inherited retinal degeneration in a mouse model.

Research square·2026
Same author

Nutritional screening, assessment, and management of peri-operative gastric cancer patients: a best practice implementation project.

JBI evidence implementation·2026
Same author

Infiltrating Monocyte Fate Switch in Retinal Degeneration: From Early Pathology to Late Homeostasis.

Research square·2026
Same author

Utilization of Robust Zr-Based Metal-Organic Framework for Efficient N<sub>2</sub>/H<sub>2</sub> Separation.

Materials (Basel, Switzerland)·2026
Same author

Multi-center and multi-reader comparison of abdominopelvic non-contrast and contrast-enhanced CT in the postoperative surveillance of gastrointestinal stromal tumors.

Quantitative imaging in medicine and surgery·2026
Same author

Comparative genomics and chemical inactivation analysis of three Limosilactobacillus fermentum phages.

Food microbiology·2026

Related Experiment Video

Updated: May 20, 2026

Efficient Dissection and Culture of Primary Mouse Retinal Pigment Epithelial Cells
08:33

Efficient Dissection and Culture of Primary Mouse Retinal Pigment Epithelial Cells

Published on: February 10, 2021

A2E accumulation influences retinal microglial activation and complement regulation.

Wenxin Ma1, Steven Coon, Lian Zhao

  • 1Unit on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Neurobiology of Aging
|July 24, 2012
PubMed
Summary

Accumulation of A2E, a lipofuscin component, activates retinal microglia and impairs their protective functions. This suggests a mechanism for immune dysregulation in age-related macular degeneration.

More Related Videos

Digestion of Whole Mouse Eyes for Multi-Parameter Flow Cytometric Analysis of Mononuclear Phagocytes
09:58

Digestion of Whole Mouse Eyes for Multi-Parameter Flow Cytometric Analysis of Mononuclear Phagocytes

Published on: June 17, 2020

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment
09:33

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment

Published on: September 13, 2016

Related Experiment Videos

Last Updated: May 20, 2026

Efficient Dissection and Culture of Primary Mouse Retinal Pigment Epithelial Cells
08:33

Efficient Dissection and Culture of Primary Mouse Retinal Pigment Epithelial Cells

Published on: February 10, 2021

Digestion of Whole Mouse Eyes for Multi-Parameter Flow Cytometric Analysis of Mononuclear Phagocytes
09:58

Digestion of Whole Mouse Eyes for Multi-Parameter Flow Cytometric Analysis of Mononuclear Phagocytes

Published on: June 17, 2020

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment
09:33

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment

Published on: September 13, 2016

Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • Age-related macular degeneration (AMD) is an outer retinal disease linked to aging and immune dysfunction.
  • In aging retinas, microglia accumulate lipofuscin deposits, potentially altering their function.
  • A2E is a primary bisretinoid component of ocular lipofuscin.

Purpose of the Study:

  • To investigate if A2E accumulation affects retinal microglia physiology in ways relevant to AMD.
  • To understand the cellular mechanisms underlying microglial dysfunction in AMD pathogenesis.

Main Methods:

  • Cultured retinal microglia were exposed to sublethal A2E accumulations.
  • Microglial activation, neuroprotection, chemokine receptor expression, chemotaxis, and complement regulation were assessed.

Main Results:

  • Sublethal A2E accumulation increased microglial activation and reduced neuroprotection of photoreceptors.
  • A2E decreased microglial chemokine receptor expression and suppressed chemotaxis.
  • A2E altered complement regulation, increasing complement factor B and decreasing complement factor H, promoting complement activation.

Conclusions:

  • Ocular lipofuscin accumulation in microglia contributes to outer retinal immune dysregulation in AMD.
  • Microglia play a key role in regulating local complement activation in the retina.
  • Age-related lipofuscin buildup in microglia is a potential cellular mechanism driving AMD pathogenesis.