June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Meibomian Gland Dysfunction: Role of PPAR-gamma
Author Affiliations & Notes
  • Mindy Call
    University of Cincinnati, Cincinnati, Ohio, United States
  • Winston W Y Kao
    University of Cincinnati, Cincinnati, Ohio, United States
  • Jared Ebert
    University of Cincinnati, Cincinnati, Ohio, United States
  • Footnotes
    Commercial Relationships   Mindy Call, None; Winston Kao, None; Jared Ebert, None
  • Footnotes
    Support  NIH/NEI EY013755, EY011845, Ohio Lions Eye Research Foundation.
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 4394. doi:
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      Mindy Call, Winston W Y Kao, Jared Ebert; Meibomian Gland Dysfunction: Role of PPAR-gamma
      . Invest. Ophthalmol. Vis. Sci. 2017;58(8):4394.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Meibomian gland dysfunction is characterized by changes in glandular secretion and/or terminal duct obstruction resulting from a chronic abnormality of the meibomian glands. This results in chronic inflammation, dry eye, or other ocular surface diseases. The meibomian glands are responsible for secreting a majority of the lipids that compromise the tear film. PPAR-gamma is involved in lipid metabolism, cellular proliferation and adipogenesis and is considered to be a terminal differentiation marker of meibocytes. In addition to these roles, PPAR-gamma has also been shown to have anti-inflammatory properties. Given these functions, the purpose of this study is to explore the role of PPAR-gamma in inflammation and lipid production and how alteration in expression can lead to pathogenesis.

Methods : An inducible, transgenic mouse model utilizing a Krt4-rtTA driver mouse was used to ablate PPAR-gamma from the ocular surface. Mice were induced at E0, P7 and P21 to assess the role of PPAR-gamma at various stages of meibomian gland development. Mice were examined for signs of meibomian gland dysfunction/evaporative dry eye as well as the expression of meibomian gland differentiation markers and inflammation.

Results : Loss of PPAR-gamma from the ocular surface resulted in gland dropout and atrophy as determined by oil red O staining. This was more pronounced at the earlier stages of induction. Additionally mice lacking PPAR-gamma, resulted in corneal opacity and compromised barrier function. Prolonged periods of induction resulted in inflammation as seen by an increase in CD45 expression.

Conclusions : Use of the Krt4-rtTA driver mouse to remove PPAR-gamma resulted in meibomian gland dysfunction/evaporative dry eye disease. PPAR-gamma helps to maintain the health of the ocular surface by maintaining meibocyte differentiation and prevention of inflammation.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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