The proliferative and migratory activities of trabecular meshwork cells

Grierson, Ian; Hogg, Penny

doi:10.1016/1350-9462(95)00002-x

Cited by 31 publications

(23 citation statements)

References 95 publications

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“…70 It has been speculated that by removing debris from the circulating aqueous, the meshwork cells behave as a biological filter preventing the deposition of such materials. In fact, phagocytosis can lead to functional problems in various forms of secondary glaucoma and even primary open-angle glaucoma.…”

Section: Latanoprost and The Outflow Systemmentioning

confidence: 99%

Latanoprost and Pigmentation

2004

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Latanoprost is a prostaglandin analogue with well-established efficacy in the treatment of open-angle glaucoma and ocular hypertension. Once-daily administration of this drug for up to 5 years is generally well tolerated both locally and systemically. While most reported side effects have been classified as mild in intensity, an increase in iris, eyelash, and periocular pigmentation has been associated with prostaglandin analogue use in some patients. Follow-up studies of patients withdrawn from latanoprost treatment suggest that the increased iridial pigmentation is irreversible while changes in eyelash and periocular skin pigmentation are reversible after cessation of therapy. Concern as to whether latanoprost affects proliferation of iridial melanocytes or other cellular components prompted investigation into its mechanism of action. All available evidence from in vitro, in vivo, and clinical studies suggests that latanoprost does not induce melanocyte proliferation. Morphologic study of human peripheral iridectomy specimens did not reveal any significant latanoprost-induced pathologic change in the iris. There was no evidence of melanin granules blocking the outflow pathways in treated patients. Stimulation of melanogenesis in iridial melanocytes, perhaps through an effect on tyrosinase, appears to account for induction of melanin production. Additional studies are in progress to further elucidate the mechanism of latanoprost-induced increased iridial pigmentation.

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Section: Latanoprost and The Outflow Systemmentioning

confidence: 99%

Latanoprost and Pigmentation

2004

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“…TM cells are gradually lost throughout life in all individuals and, under normal circumstances, they are not replaced (15). A number of studies have demonstrated that loss of TM cells is higher in POAG patients than in age-matched controls (16)(17)(18).…”

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confidence: 99%

Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo

Zhu

Gramlich

Laboissonniere

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

133

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Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction and loss of the postmitotic cells residing within this tissue. To determine if IOP control can be maintained by replacing lost TM cells, we transplanted TM-like cells derived from induced pluripotent stem cells into the anterior chamber of a transgenic mouse model of glaucoma. Transplantation led to significantly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk. The ability to maintain normal IOP engendered survival of retinal ganglion cells, whose loss is ultimately the cause for reduced vision in glaucoma. In vivo and in vitro analyses demonstrated higher TM cellularity in treated mice compared with littermate controls and indicated that this increase is primarily because of a proliferative response of endogenous TM cells. Thus, our study provides in vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel approaches in the treatment of this disease.G laucoma is one of the most common causes of irreversible vision loss and blindness worldwide; ∼60 million suffer from this disease, and of these, 7 million are blind (1). By definition all glaucoma involves some degree of vision loss, which is because of the death of retinal ganglion cells (RGC), as well as degeneration of the optic nerve head, the optic nerve, and the lateral geniculate nucleus (2, 3). Advanced age and elevated intraocular pressure (IOP) are the two most significant risk factors for the development of glaucoma. Elevated IOP is typically a result of disturbances in the balance of aqueous humor production and drainage. Aqueous humor is continuously synthesized within the eye and drained primarily through the trabecular meshwork (TM), a specialized structure located anterior to the root of the iris. Although occlusion of the aqueous humor outflow pathways can occur through several mechanisms, in the United States and other Western populations the most common form of glaucoma is primary open angle glaucoma (POAG), which manifests no gross abnormalities to the anterior portion of the eye.Randomized clinical trials have shown that reduction of IOP slows the onset and progression of glaucoma, even in patients without suspicious elevation of IOP (4, 5). Although there has been increasing awareness that factors other than elevated IOP contribute to glaucomatous damage, to date all treatments for glaucoma remain aimed at reducing IOP either through surgical or medical means, which has resulted in significant preservation of vision and increased quality of life for millions of glaucoma patients (6, 7).Although the TM in eyes with POAG appears relatively normal at a gross morphological level, a number of more subtle changes influencing the mechanical properties of the TM collage...

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“…Moreover, depletion of TM cells is considered to play a pivotal role within the factors conferring the development of primary open-angle glaucoma (POAG). In fact, the age-related TM cell loss is even more pronounced in patients with primary open-angle glaucoma (POAG) than in agematched normals [14][15][16][17]. In this context detachment from the trabeculae and migration from 5 Recently, the TM has been implicated as a target of cannabinoid action.…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

Ramer

Hinz

2010

Biochemical Pharmacology

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To cite this version:Robert Ramer, Burkhard Hinz. Cyclooxygenase-2 AND tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells. Biochemical Pharmacology, Elsevier, 2010, 80 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 ABSTRACTCannabinoids have received considerable attention as potential antiglaucomatous drugs.

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The proliferative and migratory activities of trabecular meshwork cells

Cited by 31 publications

References 95 publications

Latanoprost and Pigmentation

Latanoprost and Pigmentation

Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

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