Ma C, Papermaster D, Cepko C L
Howard Hughes Medical Institute and Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9938-43. doi: 10.1073/pnas.95.17.9938.
Cyclin D1-deficient mice have small eyes with thin retinas. We observed that there was a lower level of retinal cell proliferation and a unique pattern of photoreceptor cell death. Death was first observed in scattered clusters of cells in the retina. It then appeared to spread from these few cells to nearby photoreceptors, eventually producing extensive holes in the photoreceptor layer. These holes appeared to be filled with interneurons from the inner nuclear layer. The death mainly occurred during the second to fourth postnatal weeks. Other models of photoreceptor degeneration in rodents differ in that they occur more uniformly across the retina, with death proceeding over a longer period of time until all, or nearly all, of the photoreceptors degenerate. We also tested whether expression of a bcl-2 transgene could prevent the death and found that it could not.
细胞周期蛋白D1缺陷型小鼠眼睛小,视网膜薄。我们观察到视网膜细胞增殖水平较低,且光感受器细胞死亡模式独特。死亡首先在视网膜中散在的细胞簇中观察到。然后似乎从这少数细胞扩散到附近的光感受器,最终在光感受器层产生广泛的空洞。这些空洞似乎被来自内核层的中间神经元填满。死亡主要发生在出生后第二至第四周。啮齿动物光感受器退化的其他模型不同之处在于,它们在视网膜上更均匀地发生,死亡持续较长时间,直到所有或几乎所有光感受器退化。我们还测试了bcl-2转基因的表达是否能预防死亡,发现不能。