Department of Ophthalmology & Visual Science, University of Texas Health Science Center at Houston Medical School, Houston, Texas 77030, USA.
J Neurosci. 2012 Sep 12;32(37):12797-807. doi: 10.1523/JNEUROSCI.0118-12.2012.
Unlike many other vertebrates, a healthy mammalian retina does not grow throughout life and lacks a ciliary margin zone capable of actively generating new neurons. The isolation of stem-like cells from the ciliary epithelium has led to speculation that the mammalian retina and/or surrounding tissues may retain neurogenic potential capable of responding to retinal damage. Using genetically altered mouse lines with varying degrees of retinal ganglion cell loss, we show that the retinal margin responds to ganglion cell loss by prolonging specific neurogenic activity, as characterized by increased numbers of Atoh7(LacZ)-expressing cells. The extent of neurogenic activity correlated with the degree of ganglion cell deficiency. In the pars plana, but not the retinal margin, cells remain proliferative into adulthood, marking the junction of pars plana and retinal margin as a niche capable of producing proliferative cells in the mammalian retina and a potential cellular source for retinal regeneration.
与许多其他脊椎动物不同，健康的哺乳动物视网膜在其一生中不会生长，并且缺乏能够主动产生新神经元的睫状缘区。从睫状上皮中分离出具有干细胞样特征的细胞，这使得人们推测哺乳动物的视网膜和/或周围组织可能保留有神经发生潜能，能够对视网膜损伤做出反应。利用具有不同程度的视网膜神经节细胞损失的基因改变的小鼠系，我们发现视网膜边缘通过延长特定的神经发生活性来响应神经节细胞损失，其特征是 Atoh7(LacZ)-表达细胞的数量增加。神经发生活性的程度与神经节细胞缺乏的程度相关。在平面部，但不在视网膜边缘，细胞在成年期仍然具有增殖能力，这标志着平面部和视网膜边缘的交界处是一个能够在哺乳动物视网膜中产生增殖细胞的龛位，也是视网膜再生的潜在细胞来源。
