Human Posterior Subcapsular Cataract

Eshaghian, Joseph; Streeten, Barbara W.

doi:10.1001/archopht.1980.01020030136016

Cited by 101 publications

(21 citation statements)

References 14 publications

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“…6). The morphological characteristics of cells at the posterior of this lens were similar to published descriptions of human PSCs (Streeten and Eshaghian, 1978; Eshaghian and Streeten, 1980) and resembled the PSCs in Trp53 CKO mouse lenses. Large eosinophilic ‘balloon’ cells filled the posterior fiber mass and epithelioid cells adhered to the posterior capsule in the human eye (Fig.…”

Section: Resultssupporting

confidence: 82%

“…Epithelial cells might fail to differentiate into fiber cells at the lens equator. The resulting ‘epithelioid’ cells migrate along the inner surface of the posterior capsule, accumulate near the posterior pole of the lens and scatter light, resulting in cataract formation (Streeten and Eshaghian, 1978; Eshaghian and Streeten, 1980). Alternatively, a small fraction of the elongating fiber cells might fail to exit the cell cycle, undergo mitosis, and escape ‘execution’ by p53.…”

Section: Discussionmentioning

confidence: 99%

“…Posterior subcapsular cataracts (PSCs) are one of the three main types of age-related cataracts, although the mechanisms of PSC formation have rarely been studied and remain poorly understood. It has long been thought that PSCs might occur as a result of abnormal proliferation and migration of epithelial cells or the failure of proper terminal differentiation of fiber cells (Streeten and Eshaghian, 1978; Eshaghian and Streeten, 1980). …”

Section: Introductionmentioning

confidence: 99%

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The tumor suppressor geneTrp53protects the mouse lens against posterior subcapsular cataracts and the BMP receptor Acvr1 acts as a tumor suppressor in the lens

Wiley

Rajagopal²,

Dattilo³

et al. 2011

Disease Models &Amp; Mechanisms

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SUMMARYWe previously found that lenses lacking the Acvr1 gene, which encodes a bone morphogenetic protein (BMP) receptor, had abnormal proliferation and cell death in epithelial and cortical fiber cells. We tested whether the tumor suppressor protein p53 (encoded by Trp53) affected this phenotype. Acvr1 conditional knockout (Acvr1CKO) mouse fiber cells had increased numbers of nuclei that stained for p53 phosphorylated on serine 15, an indicator of p53 stabilization and activation. Deletion of Trp53 rescued the Acvr1CKO cell death phenotype in embryos and reduced Acvr1-dependent apoptosis in postnatal lenses. However, deletion of Trp53 alone increased the number of fiber cells that failed to withdraw from the cell cycle. Trp53CKO and Acvr1;Trp53DCKO (double conditional knockout), but not Acvr1CKO, lenses developed abnormal collections of cells at the posterior of the lens that resembled posterior subcapsular cataracts. Cells from human posterior subcapsular cataracts had morphological and molecular characteristics similar to the cells at the posterior of mouse lenses lacking Trp53. In Trp53CKO lenses, cells in the posterior plaques did not proliferate but, in Acvr1;Trp53DCKO lenses, many cells in the posterior plaques continued to proliferate, eventually forming vascularized tumor-like masses at the posterior of the lens. We conclude that p53 protects the lens against posterior subcapsular cataract formation by suppressing the proliferation of fiber cells and promoting the death of any fiber cells that enter the cell cycle. Acvr1 acts as a tumor suppressor in the lens. Enhancing p53 function in the lens could contribute to the prevention of steroid- and radiation-induced posterior subcapsular cataracts.

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Section: Resultssupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The tumor suppressor geneTrp53protects the mouse lens against posterior subcapsular cataracts and the BMP receptor Acvr1 acts as a tumor suppressor in the lens

Wiley

Rajagopal²,

Dattilo³

et al. 2011

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

show abstract

“…This is the first study to demonstrate that PSCs associated with retinal degeneration preclude normal posterior suture formation. However, involvement of the posterior sutures in PSC formation was previously inferred from the stellate pattern of opacity present in cataracts associated with aging and myotonic dystrophy (Eshaghian, 1982). These findings strongly suggest that a failure to form normal posterior sutures is a critical component in PSCs from a variety of etiologies.…”

Section: Discussionmentioning

confidence: 38%

The Structure Of Posterior Subcapsular Cataracts In The Royal College Of Surgeons (RCS) Rats

Al-Ghoul

Novak

Kuszak

1998

Experimental Eye Research

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“…In the cells exposed to lower concentrations or in unexposed cells, no multilayering was evident. The appearance of multilayered HLEC after dexamethasone exposure is indicative of a dysregulation of proliferation, differentiation or migration of the cells, all of which have been discussed as pathogenic mechanisms behind PSC formation [36, 37]. Since there is a direct link between the prolonged use of steroids and this particular type of cataract, the present findings are of great importance for elucidating the mechanism behind cortisone cataract.…”

Section: Discussionmentioning

confidence: 71%

Cell Adhesion Molecule Expression in Human Lens Epithelial Cells After Corticosteroid Exposure

Celojevic

Carlsson²,

Br³

et al. 2012

TOOPHTJ

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Aim: The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells (HLEC) subjected to glucocorticoids.Methods: Human lens epithelial cells were exposed to different concentrations of dexamethasone for 24 hours. Cell adhesion molecule expression was studied by western blot and immunohistochemistry of vimentin, N-cadherin, E-cadherin, α-catenin, β-catenin and γ-catenin. Expression of the glucocorticoid receptor (GR) was also studied. Cell morphology was examined by transmission electron microscopy (TEM).Result:Expression of N-cadherin, α-catenin, β-catenin and GR was significantly decreased in dexamethasone exposed cells as compared to unexposed cells. No significant change in γ-catenin was present. Visualization of adhesion molecules, N-cadherin and α-catenin, by immunohistochemistry showed decreased antigen reactivity in dexamethasone exposed as compared to the unexposed cells. However, no change was seen for β-catenin and γ-catenin. E-cadherin was not detectable using western blot or immunohistochemistry.TEM showed multilayering of cells, vacuole formation and appearance of electron-dense multivesicular bodies in HLEC exposed to 0, 0.1, 1, 10 and 100 αM dexamethasone.Conclusion:Glucocorticoids affect several adhesion molecules in lens epithelial cells, something that may contribute to the pathogenesis of posterior subcapsular opacification.

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Human Posterior Subcapsular Cataract

Cited by 101 publications

References 14 publications

The tumor suppressor geneTrp53protects the mouse lens against posterior subcapsular cataracts and the BMP receptor Acvr1 acts as a tumor suppressor in the lens

The tumor suppressor geneTrp53protects the mouse lens against posterior subcapsular cataracts and the BMP receptor Acvr1 acts as a tumor suppressor in the lens

The Structure Of Posterior Subcapsular Cataracts In The Royal College Of Surgeons (RCS) Rats

Cell Adhesion Molecule Expression in Human Lens Epithelial Cells After Corticosteroid Exposure

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