Animal models for inherited cataracts: a review

Gelatt, Kirk N.; Das, Noveen D.

doi:10.3109/02713688409065600

Cited by 24 publications

(11 citation statements)

References 36 publications

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“…As pointed out previously, the onset or appearance of each grade of opacification was variable, but these variations were al most the same as those of other experimental animals [3,[7][8][9][10]. In the case that the mice strain used in this study did not regularly yield the same type of cataract formation, the difference in the results of cataract devel opment between previous investigations and our observations will be explained.…”

Section: Discussioncontrasting

confidence: 55%

“…Because of late onset and slow develop ment of lens opacification, this mouse seemed to be a suitable animal model for studying human senile cataract [1][2][3]. Most of the previous investigations were designed to observe initial characteristic biochemical changes which correlated with lens opacifi cation in the early stage [2], however, the course of cataract development described b\ previous authors is not the same as that ol our observation.…”

Section: Introductioncontrasting

confidence: 55%

“…Initial opacification appears about the 3rd to 5th week after birth in Nakano, Philly and Deer mice and at the 2nd month in the Fraser mouse [3], Recent ly, the Emory mouse has also been used as an experimental animal for cataract investiga tion. Kuck et al [1] pointed out that the onset of this cataract is between the 6th and 8th months.…”

Section: Discussionmentioning

confidence: 99%

“…Cataract development seen in this experiment was different from what was described in pre vious articles, especially in the initial changes. Gelatt and Das [3] characterized and described the onset as occurring during the 6th to 8th months. In this experiment, however, the earliest onset of lens opacifica tion was found to be the end of the 4th week, and anterior cortical opacities seemed to be characteristic.…”

Section: Discussionmentioning

confidence: 99%

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In vivo Observations of Cataract Development in Emory Mouse

Takizawa¹,

Sasaki²

1986

Ophthalmic Res

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In order to establish staging of cataract development in Emory mice, in vivo observation of crystalline lenses of 366 eyes in 183 Emory mice were performed with the slit-lamp microscope from the time of opening of the lid fissure to the age of 12 months. The findings were documented by conventional slit-lamp photography and a Scheimpflug camera and were analyzed by the same methods used for human eyes. The cataract development was divided into four stages. Initial opacification in the central part of the anterior superficial cortex appeared until the 2nd month of age (stage I). In stage II, opacification progressed into the deep cortex which was seen by the 6th month at the latest. In the 7th or 8th month, opalescent opacity spread around the nucleus (stage III). Stage IV was total opacification, appearing between the 10th and 12th month.

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Section: Discussioncontrasting

confidence: 55%

Section: Introductioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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In vivo Observations of Cataract Development in Emory Mouse

Takizawa¹,

Sasaki²

1986

Ophthalmic Res

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“…The results presented in this study also emphasize the importance of immortalizing functions on tissue development in vivo. Comparison of the pathology of the lens in the aPyLT mice to cataracts in mouse (Gelatt and Das 1984), guinea pig, and man (T. Kuwabara, unpubl.) may provide some insight to the molecular events responsible for these pathological conditions.…”

Section: Lack Of Hyperplasia and Tumor Formationmentioning

confidence: 99%

Perturbed development of the mouse lens by polyomavirus large T antigen does not lead to tumor formation.

Griep¹,

Kuwabara²,

Lee³

et al. 1989

Genes Dev.

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To study how the oncogenic process may involve effects on differentiation, we overexpressed an immortalizing oncogene in a developing tissue in transgenic mice. By use of a gene fusion of the aA-crystallin promoter to the viral immortalizing oncogene, polyoma large T antigen (PyLT), we created transgenic mice that express PyLT specifically in ocular lens. Expression of large T antigen during embryonic development led to a perturbation in lens development, specifically, an interference with the normal program of fiber cell differentiation. This resulted in microphthalmia, which persisted throughout the life of the animal. Histological analysis revealed impairment of cell elongation, denucleation, and mitotic senescence in both primary and secondary fiber cell differentiation. Strikingly, there was no evidence for hyperplasia or for tumor development in vivo, unlike the consequences of many immortalizing oncogenes on tissues in other transgenic mice. In vitro, however, the developmentally perturbed cells derived from the transgenic lens showed high proliferative capacity. Our results suggest that a primary effect of aberrant expression of an immortalizing gene is an interference with normal tissue development; however, this interference may not necessarily induce proliferation or lead to tumor formation.

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Cataract Due to Tryptophan Deficiency, Rat

Render¹,

Carlton²

1991

Eye and Ear

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Animal models for inherited cataracts: a review

Cited by 24 publications

References 36 publications

In vivo Observations of Cataract Development in Emory Mouse

In vivo Observations of Cataract Development in Emory Mouse

Perturbed development of the mouse lens by polyomavirus large T antigen does not lead to tumor formation.

Cataract Due to Tryptophan Deficiency, Rat

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