PPARγ-mediated advanced glycation end products regulate neural stem cell proliferation but not neural differentiation through the BDNF-CREB pathway
PPARγ-mediated advanced glycation end products regulate neural stem cell proliferation but not neural differentiation through the BDNF-CREB pathway
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DOI：
10.1016/j.toxlet.2011.07.026
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发表时间：
2011-10-30
影响因子：
3.5
通讯作者：
Huang, Yan
中科院分区：
文献类型：
--
作者：
Wang, Shao-hua;Guo, Yi-jing;Huang, Yan
目标：为探讨过氧化物酶体增殖物激活受体γ（PPARgamma）在晚期糖基化终产物（AGE）介导的神经干细胞（NSCs）特性中的作用及其分子机制，制备了表达针对PPARgamma的短发夹状RNA（shRNA）的pLentiLox3.7慢病毒载体，并转染NSCs。MTT法检测细胞生长情况，激光共聚焦扫描法检测细胞分化情况，Western blot法检测细胞内MAP 2/nestin的表达。结果：慢病毒载体介导的shRNA沉默了NSCs中PPAR γ的表达。AGE-BSA（400 mg/L和200 mg/L）组神经干细胞的增殖和BDNF通路成分的表达分别在第3天和第7天下降（均P
Aims: To investigate the roles of PPAR gamma in advanced glycation end product (AGE)-mediated characteristics of neural stem cells (NSCs) and the molecular mechanisms of action.Methods: We prepared pLentiLox3.7 lentiviral vectors expressing short hairpin RNA (shRNA) against PPAR gamma and transduced NSCs. MTT absorbance and cell counts were used to assay cell growth, and cell differentiation was analysed by confocal laser-scanning and western blots for the expression of MAP2/nestin. The protein and gene expression of the BDNF CREB pathway components were examined by western blotting and real-time PCR.Results: Immunoblot analysis indicated that shRNA delivered by lentiviral vectors silenced PPAR gamma expression in NSCs. The proliferation of NSCs and expression of BDNF pathway components dropped in AGE-BSA culture medium (400 mg/L and 200 mg/L) on Day 3 and Day 7, respectively (all P