Expression of Matrix Metalloproteinases and Their Inhibitors in Human Trabecular Meshwork Cells

Pang, Iok‐Hou; Hellberg, Peggy E.; Fleenor, Debra L.; Jacobson, Nasreen; Clark, Abbot F.

doi:10.1167/iovs.02-0756

Cited by 59 publications

(62 citation statements)

References 26 publications

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“…[105][106][107] SPARC is present in aqueous humor and is produced by trabecular meshwork endothelial cells. 108,109 SPARC-null mice reportedly display lower IOP than wild-type animals, which suggests a potential role for SPARC in regulating IOP. 110 Furthermore, investigation of two patient cohorts of Southern Chinese origin with acute and chronic PACG has led to the identification of an association between CALCRL polymorphisms and acute but not chronic PACG.…”

Section: Nebmentioning

confidence: 97%

The genetic mechanisms of primary angle closure glaucoma

Ahram

Alward

Kuehn

2015

Eye

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Primary Angle Closure Glaucoma (PACG) is one of the most common types of glaucoma affecting over 15 million individuals worldwide. Family history and ethnicity are strongly associated with the development of the disease, suggesting that one or more genetic factors contribute to PACG. Although strictly heritable disease-causing mutations have not been identified, a number of recent association studies have pointed out genetic factors that appear to contribute to an individual's risk to develop PACG. In addition, genetic factors have been identified that modify PACG endophenotypes for example, axial length. Herein we review the current literature on this important topic.

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Section: Nebmentioning

confidence: 97%

The genetic mechanisms of primary angle closure glaucoma

Ahram

Alward

Kuehn

2015

Eye

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“…There is increasing evidence suggest that the resistance to aqueous humor drainage through TM drainage tissue is in part dependent on the composition of ECM in this tissue [21,23]. For example, outflow facility increases upon exogenous introduction of MMPs into conventional tract [23] or by altering endogenously produced MMPs by conventional outflow cells [71,72]. Thus, further investigation into EP mediated effects on MMPs in the conventional outflow pathway is necessary.…”

Section: Prostaglandin Ementioning

confidence: 99%

Endogenous bioactive lipids and the regulation of conventional outflow facility

Wan

Woodward

Stamer

2008

Expert Review of Ophthalmology

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SummaryPerturbation of paracrine signaling within the human conventional outflow pathway influences tissue homeostasis and outflow function. For example, exogenous introduction of the bioactive lipids, sphingosine-1-phosphate, anandamide or prostaglandin F 2α , to conventional outflow tissues alters the rate of drainage of aqueous humor through the trabecular meshwork, and into Schlemm's canal. This review summarizes recent data that characterizes endogenous bioactive lipids, their receptors and associated signaling partners in the conventional outflow tract. We also discuss the potential of targeting such signaling pathways as a strategy for the development of therapeutics to treat ocular hypertension and glaucoma.

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“…2 Although not all of the physiologic processes responsible for the regulation of TM and ciliary body (CB) drainage are known, extracellular matrix (ECM) turnover is at least one contributory factor. [3][4][5] The mechanisms regulating the deposition and turnover of the ECM are not fully understood.…”

mentioning

confidence: 99%

Thrombospondin-1 (TSP1)–Null and TSP2-Null Mice Exhibit Lower Intraocular Pressures

Haddadin

Kang

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Thrombospondin-1 (TSP1) and TSP2 are matricellular proteins that have been shown to regulate cytoskeleton, cell adhesion, and extracellular matrix remodeling. Both TSP1 and TSP2 are found in the trabecular meshwork (TM). In cadaver eyes with primary open-angle glaucoma (POAG), TSP1 is increased in one third of patients. We hypothesized that TSP1 and TSP2 participate in the regulation of intraocular pressure (IOP).METHODS. IOPs of TSP1-null, TSP2-null mice, and their corresponding wild-type (WT) mice were measured using a commercial rebound tonometer. Fluorophotometric measurements assessed aqueous turnover. Central corneal thickness (CCT) was measured by optical coherence tomography. Iridocorneal angles were examined using light microscopy (LM), immunofluorescence (IF), and transmission electron microscopy (TEM).RESULTS. Average IOPs of TSP1-null and TSP2-null mice were 10% and 7% less than that of the corresponding WT mice, respectively. CCTs were 6.5% less in TSP1-null mice (P < 0.05) and 1.1% less in TSP2-null mice (P > 0.05). Fluorophotometric measurements suggest that aqueous turnover rates in TSP1-null and TSP2-null mice are greater than those of WT mice. LM of the TSP1-null and TSP2-null iridocorneal angles reveals morphology, which is indistinguishable from that of their corresponding WTs. IF revealed possible concurrent underexpression of TSP2 in TSP1-null mice and of TSP1 in TSP2-null mice. TEM revealed larger collagen fibril diameters in TSP1-null and TSP2-null mice compared with WTs.CONCLUSIONS. TSP1-null and TSP2-null mice have lower IOPs than their WT counterparts. The rate of aqueous turnover suggests that the mechanism is enhanced outflow facility. An alteration in the extracellular matrix may contribute to this finding. (Invest Ophthalmol Vis Sci. 2012;53:6708-6717)

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Expression of Matrix Metalloproteinases and Their Inhibitors in Human Trabecular Meshwork Cells

Abstract: The expression of the different MMPs and TIMPs in human TM cells was independently regulated. Production of MMP-3 was maximally activated by IL-1alpha. The IL-1alpha-stimulated expression of MMP-3 provides a probable mechanism for IL-1alpha-enhanced aqueous outflow.

Cited by 59 publications

References 26 publications

The genetic mechanisms of primary angle closure glaucoma

The genetic mechanisms of primary angle closure glaucoma

Endogenous bioactive lipids and the regulation of conventional outflow facility

Thrombospondin-1 (TSP1)–Null and TSP2-Null Mice Exhibit Lower Intraocular Pressures

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