Crybb2基因敲除对小鼠晶状体自噬的影响

Effects of lens autophagy in Crybb2 knockout mice

目的:研究beta-B2晶状体蛋白(CRYBB2)缺失对小鼠晶状体自噬的影响。方法:取6月龄野生型(WT)和Crybb2基因敲除型(Crybb2^KO)小鼠各6只,取晶状体组织,透射电子显微镜观察各组小鼠晶状体组织自噬的改变,用Western blot法检测两组小鼠自噬相关蛋白的相对表达量。结果:透射电子显微镜下观察发现,与WT小鼠相比,Crybb2KO小鼠晶状体核区线粒体累积明显,皮质区自噬小体数量增多。Western blot结果显示,Crybb2KO小鼠晶状体组织LC3B表达显著低于WT小鼠(0.09±0.01 vs 0.26±0.05),P62及p-mTOR表达(0.64±0.09和0.41±0.03)显著高于WT小鼠(0.43±0.07和0.27±0.02)。结论:CRYBB2晶状体蛋白缺失会影响晶状体自噬,其机制可能与mTOR信号通路的自噬相关,最终导致白内障产生。

AIM:To evaluate the effects of Beta-B2 crystallin(CRYBB2)knockout on autophagy of mouse lens.METHODS:Six-month-old WT and Crybb2^KO mice were selected respectively.The morphological changes of autophagy of lens were observed by transmission electron microscopy.The expression of autophagy related proteins in the two groups were detected by Western blot method.RESULTS:Compared with the control group,transmission electron microscopy revealed that mitochondria was accumulated and the number of autophagosomes in lens were higher in Crybb2^KO mice.The relative expression of LC3B in Crybb2^KO group was lower(0.09±0.01 vs 0.26±0.05).The P62 protein and p-mTOR(0.64±0.09 and 0.41±0.03)was higher than WT group(0.43±0.07 and 0.27±0.02).CONCLUSION:The deletion of CRYBB2 may affect the process of lens autophagy by mTOR pathway and lead to cataract formation.