Immunohistochemical evaluation of the extracellular matrix in trabecular meshwork in steroid-induced glaucoma

Tawara, Akihiko; Tou, Norihiko; Kubota, Toshiaki; Harada, Yukinori; Yokota, Kiyomi

doi:10.1007/s00417-008-0800-0

Cited by 48 publications

(22 citation statements)

References 14 publications

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“…In addition to extracellular matrix deposition in the trabecular meshwork, steroids are also associated with microstructural alterations in the meshwork and reduced phagocytic activity of meshwork endothelial cells. 1,2,14,15 Several genes, including those for myocilin, have been implicated. 2,16,17 The mechanism by which high axial myopia would predispose a patient to steroid responsiveness is unknown.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for steroid response among cataract patients

Chang¹,

Tan²,

Tripodis³

2011

Journal of Cataract and Refractive Surgery

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Section: Discussionmentioning

confidence: 99%

Risk factors for steroid response among cataract patients

Chang¹,

Tan²,

Tripodis³

2011

Journal of Cataract and Refractive Surgery

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“…The TM in eyes treated with corticosteroids has demonstrated a marked increase in the accumulation of type IV collagen and fibronectin. 9,19 Thickening of fibers of the TM can lead to a decrease in size of the pores and thus affect aqueous outflow. 9 Because there is a steady decrease in TM cells throughout life, 15 the induced changes in microstructure of the TM in a young eye, with a larger number of TM cells, may explain why younger patients are more sensitive to corticosteroid-induced elevations in IOP.…”

Section: Discussionmentioning

confidence: 99%

Risk Factors Associated With Intraocular Pressure Increase in Patients With Uveitis Treated With the Fluocinolone Acetonide Implant

Parekh

Srivastava

Bena³

et al. 2015

JAMA Ophthalmol

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IMPORTANCE Elevated intraocular pressure (IOP) is a well-known adverse event associated with the fluocinolone acetonide implant (FAI), but no data are available regarding factors associated with increased risk of IOP elevation in patients treated with the FAI.OBJECTIVE To report risk factors that may predispose patients to elevated IOP after treatment with the FAI. DESIGN, SETTING, AND PARTICIPANTS Data from 3 multicenter, 3-year, prospective, randomized, phase 2b/3 clinical trials evaluating the safety and efficacy of the FAI were pooled and analyzed. Patients had no underlying glaucoma and at least one eye with a history of recurrent noninfectious uveitis affecting the posterior segment. Patients were treated with 1 or more of the following: systemic therapy (corticosteroids or other immunosuppressive drugs) for at least 3 months before enrollment, 2 or more sub-Tenon capsule corticosteroid injections for uveitis management during the 6 months before enrollment, or systemic corticosteroid or sub-Tenon capsule corticosteroid injection therapy required for at least 2 separate recurrences within 6 months before enrollment. MAIN OUTCOMES AND MEASURESFactors evaluated as risk factors for IOP elevation included age, sex, lens status, uveitis severity at enrollment, and location of uveitis.RESULTS Data analyses were based on 641 eyes. A total of 351 eyes did not receive the FAI, whereas 290 eyes had the 0.59-mg FAI placed. An increase in IOP of 10 mm Hg or elevation to 30 mm Hg was seen in 60 untreated eyes (17.1%) and 188 treated eyes (65.1%) (hazard ratio, 5.80; 95% CI, 4.28-7.70; P < .001). A total of 8 untreated eyes (2.3%) required surgical intervention for elevated IOP compared with 93 treated eyes (32.1%) (hazard ratio, 16.48; 95% CI, 8.24-32.96; P < .001). In patients with the FAI, younger age, male sex, and phakic lens status were associated with higher risk of IOP elevation and the need for glaucoma surgery (P = .003, P < .001, and P < .001, respectively). CONCLUSIONS AND RELEVANCEPatients receiving the FAI are at higher risk of developing an IOP increase of 10 mm Hg or an absolute IOP of 30 mm Hg when compared with patients without the FAI. Patients who are male, younger, and phakic are at an even higher risk for elevated IOP and possibly glaucoma surgery.

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“…SD plaques were highly increased and there was a large accumulation of basement membrane-like material in the JCT and subendothelial layer of SC in patients with juvenile glaucoma (Furuyoshi et al, 1997). In steroid-induced glaucoma, there is an apparent accumulation of type IV collagen and fibronectin in the outer TM beams, but not in the underneath the inner wall of SC (Tawara et al, 2008). For a more in-depth description and discussion of these and other ECM changes, the readers are referred to (Tektas and Lutjen-Drecoll, 2009).…”

Section: Ecm Changes With Glaucoma and Glaucoma Therapiesmentioning

confidence: 99%

Extracellular matrix in the trabecular meshwork: Intraocular pressure regulation and dysregulation in glaucoma

Vranka

Kelley

Acott

et al. 2015

Experimental Eye Research

290

283

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The trabecular meshwork (TM) is located in the anterior segment of the eye and is responsible for regulating the outflow of aqueous humor. Increased resistance to aqueous outflow causes intraocular pressure to increase, which is the primary risk factor for glaucoma. TM cells reside on a series of fenestrated beams and sheets through which the aqueous humor flows to exit the anterior chamber via Schlemm’s canal. The outer trabecular cells are phagocytic and are thought to function as a pre-filter. However, most of the outflow resistance is thought to be from the extracellular matrix (ECM) of the juxtacanalicular region, the deepest portion of the TM, and from the inner wall basement membrane of Schlemm’s canal. It is becoming increasingly evident that the extracellular milieu is important in maintaining the integrity of the TM. Not only have ultrastructural changes been observed in the ECM of the TM in glaucoma, and a significant number of mutations in ECM genes are known to be associated with glaucoma, but the stiffness of glaucomatous TM appears to be greater than that of normal tissue. Additionally, TGFβ2 has been found to be elevated in the aqueous humor of glaucoma patients and is assumed to be involved in ECM changes deep with the juxtacanalicular region of the TM. This review summarizes the current literature on trabecular ECM as well as the development and function of the TM. Animal models and organ culture models targeting specific ECM molecules to investigate the mechanisms of glaucoma are described. Finally, the growing number of mutations that have been identified in ECM genes and genes that modulate ECM in humans with glaucoma are documented.

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Immunohistochemical evaluation of the extracellular matrix in trabecular meshwork in steroid-induced glaucoma

Abstract: The localization of ECMs in the TM is different in SG in comparison to that in POAG patients.

Cited by 48 publications

References 14 publications

Risk factors for steroid response among cataract patients

Risk factors for steroid response among cataract patients

Risk Factors Associated With Intraocular Pressure Increase in Patients With Uveitis Treated With the Fluocinolone Acetonide Implant

Extracellular matrix in the trabecular meshwork: Intraocular pressure regulation and dysregulation in glaucoma

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