Norose K, Clark J I, Syed N A, Basu A, Heber-Katz E, Sage E H, Howe C C
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
Invest Ophthalmol Vis Sci. 1998 Dec;39(13):2674-80.
To determine the role of SPARC (secreted protein, acidic, and rich in cysteine) in cataractogenesis by examining mice deficient in a matricellular protein SPARC.
Mice were rendered SPARC-deficient by a targeted disruption of the gene. Slit-lamp microscopy and histology were used to examine the eyes of SPARC-null and wild-type mice from birth to 14 months of age.
SPARC-null mice developed opacities in the posterior cortex of the eye as early as 1.5 months after birth. The diffuse cataracts appeared to progress toward the anterior cortex and reached maturity in many animals by 3.5 months of age. Early stages of cataractogenesis in SPARC-null mice included inhibition of normal lens fiber cell differentiation, degeneration of fiber cells, vacuole formation at the equator, and liquefaction of the cortex. No cataracts were detected in wild-type mice up to the age of 8 months.
The early onset of cataracts in SPARC-null mice establishes that the gene is essential to the maintenance of lens transparency.
通过研究缺乏基质细胞蛋白SPARC（分泌性蛋白质，酸性且富含半胱氨酸）的小鼠，确定SPARC在白内障形成过程中的作用。
通过基因靶向破坏使小鼠缺乏SPARC。使用裂隙灯显微镜检查和组织学方法，对出生至14个月大的SPARC基因敲除小鼠和野生型小鼠的眼睛进行检查。
SPARC基因敲除小鼠早在出生后1.5个月时，眼睛后皮质就出现了混浊。弥漫性白内障似乎向前皮质发展，许多动物在3.五岁时白内障达到成熟。SPARC基因敲除小鼠白内障形成的早期阶段包括正常晶状体纤维细胞分化受到抑制、纤维细胞变性、赤道部空泡形成以及皮质液化。在8个月龄之前，野生型小鼠未检测到白内障。
SPARC基因敲除小鼠白内障的早期发生表明该基因对于维持晶状体透明度至关重要。
