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Y. Xia, M. Mongan, H. Liu, J. Wang, W. Kao; Role of MAP3K1 in Mouse Postnatal Retinal Development. Invest. Ophthalmol. Vis. Sci. 2010;51(13):713.
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© ARVO (1962-2015); The Authors (2016-present)
Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) is essential for embryonic eyelid development. MAP3K1 ablation in mice results in characteristic eye open at birth (EOB) phenotype. We have previously shown that MAP3K1-deficient mice have postnatal retinal dysplasia independent of the eyelid defect. It remains unclear how MAP3K1 regulates retinal development.
At postnatal day 2 (P2)-P15, MAP3K1 expression is detected in the retinal pigment epithelium (RPE) and photoreceptor cells. Retinal malformation is seen at P7 in the Map3k1(-/-) mouse and punctuated and localized folding between the rods and cones and outer nuclear layer (ONL) is observed by P14-P21. Retinas of the knockout mice show increased cell proliferation at P6 and P10 and also increased cell apoptosis at P14-21. When aged to 3 months, the Map3k1(-/-) mice develop localized neo-vascularization in RPE and ONL and by 1 year old the overall ONL is thinner.
MAP3K1 may serve as a checkpoint for photoreceptor cell proliferation at earlier postnatal stages (P6-7) and uncontrolled proliferation may in turn cause photoreceptor cell apoptosis at later postnatal stages (P14-21). Abnormal proliferation and apoptosis programs in the Map3k1(-/-) mice are likely responsible for abnormal retinal development, dysplasia and ultimately degeneration.
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