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PPARγ Regulates Mouse Meibocyte Differentiation and Lipid Synthesis
James V Jester1, Eric Potma2, Donald J Brown1
1Gavin Herbert Eye Institute, University of California, Irvine, Irvine, CA.
The Ocular Surface
|August 18, 2016
Summary
Aging reduces cytoplasmic PPARγ in meibomian glands, impairing lipid synthesis. Activating PPARγ with rosiglitazone stimulates lipid production, suggesting a PPARγ pathway regulates age-related lipid synthesis decline.
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Biology
Background:
- Age-related meibomian gland atrophy is linked to reduced peroxisome proliferator-activated receptor gamma (PPARγ) expression.
- PPARγ is a lipid-sensitive nuclear receptor crucial for cellular lipid metabolism.
Purpose of the Study:
- To investigate the role of PPARγ in regulating lipid synthesis within meibocytes.
- To understand how PPARγ function changes with age in meibomian glands.
Main Methods:
- Examined PPARγ expression in meibomian glands from young and old mice.
- Cultured and immortalized mouse meibocytes to assess lipid synthesis.
- Utilized LipidTox staining and CARS/Raman microspectroscopy for lipid analysis.
- Investigated the effects of a PPARγ agonist (rosiglitazone) on meibocyte lipid synthesis, PPARγ localization, and gene expression.
Main Results:
- Young mice showed distinct PPARγ bands in cytoplasmic fractions, which were reduced in older mice.
- Cultured meibocytes synthesized neutral lipids, mimicking mouse meibum composition.
- Rosiglitazone treatment significantly increased meibocyte lipid production, correlating with PPARγ sumoylation and cytoplasmic accumulation.
- Rosiglitazone also promoted PPARγ translocation to the cytoplasm and upregulated PPARγ, ADP, and ADFP mRNA.
Conclusions:
- Confirms loss of cytoplasmic PPARγ localization in aged, atrophic meibomian glands.
- Demonstrates that PPARγ stimulates lipid synthesis in meibocytes via sumoylation and cytoplasmic translocation.
- Suggests a PPARγ-mediated pathway is downregulated in older mice, contributing to reduced lipid synthesis.
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