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Lipoxin A4 activates ALX/FPR2 receptor to regulate conjunctival goblet cell secretion.
R R Hodges1, D Li1, M A Shatos1
1Schepens Eye Research Institute/Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
Mucosal Immunology
|April 14, 2016
Summary
Lipoxin A4 (LXA4) stimulates conjunctival goblet cells to secrete mucin and maintain ocular surface homeostasis. This finding suggests LXA4 as a potential treatment for dry eye diseases.
Area of Science:
- Ophthalmology
- Cell Biology
- Immunology
Background:
- Conjunctival goblet cells are crucial for tear film mucus layer integrity.
- Dry eye and allergic conjunctivitis involve goblet cell dysfunction.
- Lipoxin A4 (LXA4) is a proresolution agonist with potential physiological roles.
Purpose of the Study:
- Investigate LXA4's effects on rat conjunctival goblet cell mucin secretion.
- Determine LXA4's impact on intracellular calcium ([Ca2+]i) levels.
- Identify signaling pathways activated by LXA4 in goblet cells.
Main Methods:
- Localized ALX/FPR2 receptor expression in goblet cells.
- Measured mucin secretion and [Ca2+]i in cultured goblet cells.
- Utilized LXA4, its stable analogs, and inhibitors to assess cellular responses.
Main Results:
- LXA4 significantly increased mucin secretion, [Ca2+]i, and ERK 1/2 activation.
- ALX/FPR2 receptor blockade inhibited LXA4-mediated functions.
- LXA4 activated phospholipases C, D, A2, PKC, ERK 1/2, and CaMK pathways.
Conclusions:
- Conjunctival goblet cells express functional ALX/FPR2 receptors.
- LXA4 promotes goblet cell mucin secretion and calcium signaling.
- LXA4 plays a role in ocular surface homeostasis and may treat dry eye.
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