Pressures in the juxtacanalicular tissue and Schlemm's canal in monkeys

Mäepea, Olav; Bill, Anders

doi:10.1016/0014-4835(92)90151-h

Cited by 261 publications

(180 citation statements)

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“…(Bradley et al 1998) The microcapillary observations mentioned earlier also argue for the JCT ECM and against SC inner wall cells. (Maepea and Bill 1992) However, due to the highly interdependent nature of the bidirectional interactions between cells and their ECMs, an approach which can clearly differentiate between the actual direct contribution of either the cells or the ECM to the aqueous outflow resistance has not yet been devised. Consequently, although both the cells and the ECM are clearly critical to maintaining the outflow resistance, their respective direct contributions remain unclear.…”

Section: Segmental Flowmentioning

confidence: 99%

“…The figure is modified from several sources. (Tripathi 1971(Tripathi , 1977Grierson et al 1978;Rohen 1983;Grierson and Calthorpe 1989;Epstein and Rohen 1991;Maepea and Bill 1992;Lutjen-Drecoll 1999;Parc et al 2000) Fibronectin repeat type I, II and III domains, binding sites and alternative splicing. RGD, synergy and IDAPS sequences bind α5β1 and α4β1 integrins.…”

Section: Glaucoma and Ecmmentioning

confidence: 99%

“…1). (Tripathi 1971;Inomata et al 1972;Tripathi 1977;Grierson et al 1978;Rohen 1983;Grierson and Calthorpe 1989;Epstein and Rohen 1991;Maepea and Bill 1992;Lutjen-Drecoll and Rohen 1994;Lütjen-Drecoll and Rohen 1996;Lutjen-Drecoll 1999;Parc et al 2000) These JCT cells form occasional contacts with each other, often via extended processes using gap and adherens junctions. (Inomata et al 1972;Grierson et al 1978) They also form similar junctions with SC inner wall endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…(Fuchshofer et al 2006) Possible sites of the outflow resistance Sequential serial dissection and microcapillary studies with perfused eyes suggest that the trabecular outflow resistance resides somewhere within the deepest 1/4 to 1/3 of the TM. (Grant 1958;Grant 1963;Ellingsen and Grant 1972;Rosenquist et al 1989;Maepea and Bill 1992;Bill and Maepea 1994) When a microcapillary was inserted from Schlemm's canal toward the anterior chamber, the resistance was bypassed at 7-14 µm from the inner wall of Schlemm's canal. This is approximately the thickness of the juxtacanalicular region (Fig.…”

Section: Introductionmentioning

confidence: 99%

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Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

419

443

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The extracellular matrix (ECM) of the trabecular meshwork (TM) is thought to be important in regulating intraocular pressure (IOP) in both normal and glaucomatous eyes. IOP is regulated primarily by a fluid resistance to aqueous humor outflow. However, neither the exact site nor the identity of the normal resistance to aqueous humor outflow has been established. Whether the site and nature of the increased outflow resistance, which is associated with open-angle glaucoma, is the same or different from the normal resistance is also unclear.The ECMs of the TM beams, juxtacanalicular region (JCT) and Schlemm's canal (SC) inner wall are comprised of fibrillar and non-fibrillar collagens, elastin-containing microfibrils, matricellular and structural organizing proteins, glycosaminoglycans (GAGs) and proteoglycans. Both basement membranes and stromal ECM are present in the TM beams and JCT region. Cell adhesion proteins, cell surface ECM receptors and associated binding proteins are also present in the beams, JCT and SC inner wall region.The outflow pathway ECM is relatively dynamic, undergoing constant turnover and remodeling. Regulated changes in enzymes responsible for ECM degradation and biosynthetic replacement are observed. IOP homeostasis, triggered by pressure changes or mechanical stretching of the TM, appears to involve ECM turnover. Several cytokines, growth factors and drugs, which affect the outflow resistance, change ECM component expression, mRNA alternative splicing, cellular cytoskeletal organization or all of these. Changes in ECM associated with open-angle glaucoma have been identified.

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Section: Segmental Flowmentioning

confidence: 99%

Section: Glaucoma and Ecmmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Extracellular matrix in the trabecular meshwork

Acott

Kelley

2008

Experimental Eye Research

419

443

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“…TGF-β1 has been reported to be a powerful inductor of IL-6 IL-6 is known to modulate vascular permeability through different mechanisms, including increased permeability of the vascular endothelium and the induction of MMP production, which results in ECM degradation. The observed increase in outflow facility induced by IL-6 in perfused anterior segments of porcine eyes could potentially be mediated by similar mechanisms.The site of aqueous humor resistance in the human SC/TM outflow pathway has been localized to the JCT and inner wall of SC [5,12,28,[48][49][50][51]. Although the outflow pathway of porcine eyes does not contain a true SC, it shows more features in common with that of the human eye than other species [52].…”

mentioning

confidence: 99%

Induction of IL-6 expression by mechanical stress in the trabecular meshwork

Liton

Luna

Bodman

et al. 2005

Biochemical and Biophysical Research Communications

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The trabecular meshwork (TM)/Schlemm's canal (SC) outflow pathway is the tissue responsible for maintaining normal levels of intraocular pressure. In the present study, we investigate the effects of mechanical stress on the expression of IL-6 in the TM meshwork, as well as the effects of this cytokine on outflow pathway function. Application of cyclic mechanical stress to human TM primary cultures resulted in a statistically significant increase in both secretion and transcription of IL-6, compared to nonstressed controls. Addition of TGF-β1, which has been reported to be upregulated in TM cells under mechanical stress, also induced a significant activation of both the transcription and secretion of IL-6. Moreover, anti-TGF-b1 antibodies partially blocked the stretch-induced IL-6 production. Injection of IL-6 into perfused porcine anterior segments resulted in a 30% increase in outflow facility, as well as increased permeability through SC cell monolayers. These results suggest a role for IL-6 in the homeostatic modulation of aqueous humor outflow resistance. KeywordsTrabecular meshwork; Interleukin-6; Mechanical stress; TGF-β1; glaucomaThe trabecular meshwork (TM)/Schlemm's canal (SC) outflow pathway system constitutes the main route by which the aqueous humor exits the anterior chamber of the eye [1]. Maintenance of appropriate levels of aqueous humor outflow resistance through this pathway is critical in sustaining normal levels of intraocular pressure (IOP) [2,3]. Although it has been hypothesized that the TM/SC outflow pathway may respond to transient changes in IOP by altering its resistance to aqueous humor [4][5][6], thereby maintaining normal IOP levels, there is little experimental evidence explaining such potential homeostatic mechanisms.As a result of cyclic fluctuations of IOP with each heartbeat, the conventional outflow pathway is subjected to continuous cycles of stretch and relaxation that might be involved in tissue homeostasis and, consequently, in IOP regulation [7]. It has been well described that changes in IOP exert dramatic effects on the morphology of the outflow pathway [8][9][10][11][12]. Increased IOP results in distention and stretching of the outflow pathway and its contained cells, while decreased IOP leads to relaxation of the tissue. It has also been demonstrated that mechanical stress can trigger certain responses in TM cells, including cytoskeletal changes, induction of gene expression, and activation of regulatory pathways [13][14][15][16][17][18][19][20][21] One of the reported responses to increased IOP in perfused human anterior segments observed by gene array analysis is an increase in interleukin-6 (IL-6) mRNA [16]. IL-6 is well known to increase the permeability of vascular endothelium through effects on the paracellular pathway, induction of matrix metalloproteinases (MMPs), and vesicular trafficking [22][23][24]. This array of effects mediated by IL-6 suggests that this cytokine could affect aqueous humor outflow resistance in the outflow pathway by increasing ...

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Viscocanalostomy in Rhesus Monkeys

Tamm¹

2004

Arch Ophthalmol

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Objective: To examine structural changes and aqueous humor outflow after viscocanalostomy in live normal monkey eyes.Methods: Viscocanalostomy surgery was performed in 1 eye of each of 4 rhesus monkeys. Outflow facility was determined before and after surgery. All eyes were fixed and examined by light and/or electron microscopy 36 or 63 days postoperatively.Results: Schlemm canal was replaced by scar tissue at the surgical site. The juxtacanalicular zone contained homogeneous material, probably high-molecular-weight 1.4% sodium hyaluronate. The sclera external to Schlemm canal was overhydrated, and remains of a scleral lake were present in 1 animal. Multiple defects were present in the endothelial lining of Schlemm canal inner and outer wall. Fine fibrillar material and sheath-derived plaque material partly bridged the defects. Along the inner wall, aggregations of thrombocytes covered some defects in the endothelial lining of the canal. At 90°to 180°from the surgical site, small and fewer breaks in the inner wall were seen. Postsurgery outflow facility (n=2) was approximately 30% higher in the treated eye than in the contralateral control, corrected bilaterally for presurgery baseline. Conclusions:The most likely explanations for the increase in outflow facility in monkeys after viscocanalostomy are focal disruptions of the inner wall endothelium of Schlemm canal and disorganization of the juxtacanalicular zone, resulting in direct communication of juxtacanalicular zone extracellular spaces with the lumen of Schlemm canal. The continuous presence of sodium hyaluronate might prevent repair of these defects by interfering with thrombocyte function.Clinical Relevance: In nonhuman primates, viscocanalostomy appears to decrease outflow resistance through persisting focal disruption of the inner wall endothelium and opening of the juxtacanalicular or cribriform region of the trabecular meshwork, the tissue most affected by pathologic changes in primary open-angle glaucoma in humans.

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Pressures in the juxtacanalicular tissue and Schlemm's canal in monkeys

Cited by 261 publications

References 10 publications

Extracellular matrix in the trabecular meshwork

Extracellular matrix in the trabecular meshwork

Induction of IL-6 expression by mechanical stress in the trabecular meshwork

Viscocanalostomy in Rhesus Monkeys

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