Prostaglandin induces the expression of matrix metalloproteinase-1 in ciliary melanocytes.
- Author:
Ning-li WANG
1
;
Qing-jun LU
;
Jun-hong LI
;
Ling WANG
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Ciliary Body; cytology; drug effects; enzymology; Female; Fluorescent Antibody Technique; Humans; Immunoblotting; Male; Matrix Metalloproteinase 1; analysis; Melanocytes; drug effects; enzymology; Prostaglandins F, Synthetic; pharmacology
- From: Chinese Medical Journal 2008;121(13):1173-1176
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDLatanoprost, a prostaglandin F2alpha analog, has been shown to be an effective intraocular pressure lowering agent which acts by inducing ciliary muscle cells to synthesise matrix metalloproteinases. However, the response of ciliary melanocytes to latanoprost has never been reported. This research has investigated the ability of latanoprost to induce matrix metalloproteinase-1 expression in human ciliary melanocytes, and thereby advance the understanding of the mechanism of PGF(2alpha) in decreasing intraocular pressure.
METHODSIn vitro human ciliary melanocytes were treated for 48 hours with five different concentrations of latanoprost (100, 150, 200, 500, and 1000 nmol/L). Ciliary melanocytes treated with 0.01% ethanol (vehicle) were used as a control. The expression of matrix metalloproteinase-1 in ciliary melanocytes was determined by Western blotting and immunofluorescent staining.
RESULTSWestern blotting showed that the expression of matrix metalloproteinase-1 in ciliary melanocytes was induced by latanoprost, and the level of expression was dependent on the concentration of latanoprost in the culture medium. Immunofluorescent staining showed that matrix metalloproteinase-1 was confined to the ciliary melanocyte cytoplasm.
CONCLUSIONSLatanoprost induced the expression of matrix metalloproteinase-1 in human ciliary melanocytes in a dose-dependent manner. Ciliary melanocytes, as well as ciliary muscle cells, may also play an important role in uveoscleral outflow modulation.