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Editors Selection IGR 11-4

Medical Treatment: Basic latanoprost

Comment by Douglas Rhee on:

13668 Latanoprost induces matrix metalloproteinase-1 expression in human nonpigmented ciliary epithelial cells through a cyclooxygenase-2-dependent mechanism, Hinz B; Rosch S; Ramer R et al., FASEB Journal, 2005; 19: 1929-1931

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By augmenting aqueous outflow drainage, prostaglandin analogues, such as latanoprost, modify the underlying pathophysiology of elevated intraocular pressure, i.e., abnormal drainage. Other investigators have shown that latanoprost induces a matrix metalloproteinase mediated increase in extracellular matrix (ECM) turnover in both the ciliary body and trabecular meshwork. The net physiologic result of these biochemical changes is the augmentation of uveoscleral outflow with a modest enhancement of trabecular drainage. Latanoprost is an important model system to understand one of the primary mechanisms of aqueous outflow resistance regulation- turnover of ECM. Hinz et al. (521 investigated the effect of latanoprost on the production of cyclooxygenase-2 (COX-2) dependent endogenous prostaglandins and its possible association with the induction of MMPs in human non-pigmented ciliary body epithelial (NPE) cells; the cells involved with the production of aqueous humor. By using carefully designed experiments with selective inhibitory molecules, the authors found that latanoprost induces COX-2 expression as well as PGE₂ and mitogen-activated protein kinase (MAPKs) p42/44. The authors also showed that matrix metalloproteinase-1 (MMP-1) transcription is dependent on the COX-2 pathway. Interestingly, MMP-2, MMP-9, and tissue inhibitors of metalloproteinase-1 (TIMP-1) and TIMP-2 were not affected by latanoprost.

The results of this paper further delineate the breadth of biochemical responses to latanoprost and expand our understanding of the intracellular signaling pathways that mediate latanoprost's response.

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