Sun M S, Song Y Z, Zhang F J, Tao J, Liu Y B
Beijing Tongren Eye Center, Beijing Tongren Hospital of Capital Medical University, Beijing Key Lab. of Ophthalmology & Visual Sciences, Beijing 100730, China.
Zhonghua Yan Ke Za Zhi. 2016 Nov 11;52(11):850-855. doi: 10.3760/cma.j.issn.0412-4081.2016.11.009.
To investigate ocular changes in the monocularly deprivation myopic model of mutant Lumican transgenic mice. Comparing influences on biological parameters and sclera development between Lumican transgenic and form deprivation mice, and to prepare for further study of pathogenesis of pathological myopia (PM). Experimental research. Lumican transgenic mice and wild mice were monocularly lid-sutured at ten days after birth. All eyes were divided into 6 groups, group A(32 eyes): control eyes in transgenic mice; group B(34 eyes): sutured eyes in transgenic mice; group C(34 eyes): fellow eyes in transgenic mice; group D(28 eyes): control eyes in wild mice; group E(32 eyes): sutured eyes in wild mice; group F(32 eyes): fellow eyes in wild mice. Refraction was measured by streak retinoscopye and axial length was measured by vernier caliper at 8 weeks (56 days) after birth. Lumican expression was detected by quantitative real-time PCR in all groups. The refraction in group B and group E were (-0.38±1.10) D and (0.14±1.26)D respectively, which were significantly different compared with contralateral groups and normal control groups (9.525, 10.067; 0.01). The mean axial length were also increased in group B ((3.28 ± 0.07)mm and group E (3.24 ± 0.09)mm, (7.183, 6.671; 0.05). Expression level of Lumican mRNA in sclera was increased in group B, which was significantly different from group A and group C ( 6.262; 0.05). The expression of Lumican mRNA was increased in group B and C when compared with group E and F (4.772, 2.218, 0.05). Form-deprivation in mutant Lumican transgenic mice causes myopic changes in deprived eyes. The gene expression level of Lumican in sclera of transgenic mice is significantly increased compared with contralateral eyes or that of wild group. Lumican mutation may effect the development of PM, and the interaction of genetic and environmental factors may lead to development of PM. .
研究突变型亮氨酸聚糖转基因小鼠单眼剥夺性近视模型的眼部变化。比较亮氨酸聚糖转基因小鼠和形觉剥夺小鼠对生物学参数和巩膜发育的影响,为进一步研究病理性近视(PM)的发病机制做准备。实验研究。将亮氨酸聚糖转基因小鼠和野生小鼠在出生后10天进行单眼眼睑缝合。所有眼睛分为6组,A组(32只眼):转基因小鼠的对照眼;B组(34只眼):转基因小鼠的缝合眼;C组(34只眼):转基因小鼠的对侧眼;D组(28只眼):野生小鼠的对照眼;E组(32只眼):野生小鼠的缝合眼;F组(32只眼):野生小鼠的对侧眼。出生后8周(56天)用带状检影法测量屈光,用游标卡尺测量眼轴长度。用定量实时PCR检测所有组的亮氨酸聚糖表达。B组和E组的屈光分别为(-0.38±1.10)D和(0.14±1.26)D,与对侧组和正常对照组相比有显著差异(9.525,10.067;P<0.01)。B组((3.28±0.07)mm)和E组(3.24±0.09)mm的平均眼轴长度也增加(7.183,6.671;P<0.05)。B组巩膜中亮氨酸聚糖mRNA的表达水平升高,与A组和C组有显著差异(6.262;P<0.05)。与E组和F组相比,B组和C组亮氨酸聚糖mRNA的表达增加(4.772,2.218,P<0.05)。突变型亮氨酸聚糖转基因小鼠的形觉剥夺导致被剥夺眼出现近视变化。转基因小鼠巩膜中亮氨酸聚糖的基因表达水平与对侧眼或野生组相比显著升高。亮氨酸聚糖突变可能影响病理性近视的发展,遗传和环境因素的相互作用可能导致病理性近视的发生。