Chaitin M H, Brun-Zinkernagel A M
Department of Anatomy and Cell Biology and North Texas Eye Research Institute, University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas, USA.
Exp Eye Res. 1998 Sep;67(3):283-92. doi: 10.1006/exer.1998.0510.
The distribution of the cell surface adhesion/receptor molecule CD44 was studied in retinas of the Royal College of Surgeons (RCS) rat which exhibits an inherited retinal dystrophy. In this animal model, the retinal pigment epithelium fails to phagocytize shed photoreceptor outer segment material, a membranous debris layer accumulates in the subretinal space and the photoreceptor cells degenerate. Using immunoperoxidase and immunogold labeling, CD44 was localized to Müller cell apical microvilli in normal rat retinas, as noted in other species. For the RCS rat, immunoperoxidase labeling of 18 day and 1 month retinas showed the typical microvillar labeling pattern. At 2 months postnatal, following degeneration of most of the photoreceptors, a more condensed band of microvillar label was observed. At 3 months, when photoreceptor degeneration was virtually complete, only distinct regions of dense label remained between the neural retina and debris zone. Upon ultrastructural and immunogold analysis, these regions were found to contain closely packed Müller cell microvilli. At all ages studied, labeling for CD44 in the inner retina did not increase, as it does in other forms of retinal degeneration which lack a debris zone. However, by 3 months the debris zone was labeled for CD44 indicating that CD44 molecules remain on Müller cell microvilli and processes which have extended into and become part of the debris zone. This may be caused by an altered distribution of still undetermined ligands for CD44 which are present within the interphotoreceptor matrix of the RCS rat retina.
研究了患有遗传性视网膜营养不良的皇家外科学院(RCS)大鼠视网膜中细胞表面粘附/受体分子CD44的分布情况。在这个动物模型中,视网膜色素上皮细胞无法吞噬脱落的光感受器外段物质,视网膜下间隙中会积累一层膜性碎片,光感受器细胞也会发生退化。与其他物种一样,利用免疫过氧化物酶和免疫金标记法,在正常大鼠视网膜中,CD44定位于Müller细胞顶端微绒毛。对于RCS大鼠,18天和1个月大的视网膜免疫过氧化物酶标记显示出典型的微绒毛标记模式。出生后2个月,在大多数光感受器退化后,观察到微绒毛标记带更加浓缩。3个月时,光感受器退化几乎完全,仅在神经视网膜和碎片区域之间存在明显的密集标记区域。通过超微结构和免疫金分析发现,这些区域含有紧密排列的Müller细胞微绒毛。在所有研究的年龄段,视网膜内层CD44的标记均未增加,而在其他缺乏碎片区域的视网膜变性形式中会增加。然而,到3个月时,碎片区域出现了CD44标记,这表明CD44分子仍存在于延伸到碎片区域并成为其一部分的Müller细胞微绒毛和突起上。这可能是由于RCS大鼠视网膜光感受器间基质中存在的尚未确定的CD44配体分布改变所致。