PPARγ介导AGEs经BDNF-CREB通路调节神经干细胞增殖
PPARγ-mediated advanced glycation end products regulate neural stem cell proliferation but not neural differentiation through the BDNF-CREB pathway
目的 探讨糖基化终产物（AGEs）影响神经干细胞（NSC）增殖和分化过程中PPARγ的作用和分子机制。 方法 构建慢病毒载体，干扰NSC的PPARγ基因表达；AGEs干预各组细胞；MTT法和神经球计数法检测细胞增殖；激光共聚焦成像和Western blot法检测细胞分化（MAP2/Nestin）；Western blot和Real-time RT-PCR法检测BDNF-CREB通路的表达。 结果 慢病毒载体能有效沉默PPARγ的表达；AGEs干预NSC后，细胞增殖和BDNF通路表达降低，沉默PPARγ的表达能逆转该效应；AGEs干预NSC后，MAP2表达减少，沉默PPARγ的表达不能逆转该效应。 结论 PPARγ介导AGEs经BDNF-CREB通路调节神经干细胞增殖，而不影响分化。
ims To investigate the roles of PPARγ in AGEs-mediated characteristics of NSC and its molecular mechanisms. Methods We prepared lentiviral vectors expressing shRNA against PPARγ and transduced NSC. MTT absorbance and cell counts were used to assay cell growth, confocal laser-scanning and western blot were used to assay cell differentiation（MAP2/Nestin）. The protein and gene expression of the BDNF-CREB pathway components were examined by western blot and real-time RT-PCR. Results PPARγ expression in NSC was silenced. The proliferation of NSC and expression of BDNF pathway components dropped in AGEs culture medium (all P＜0.001), Silencing PPARγ reversed the effects. AGEs decreased MAP2 both in NSC and PPARγ-silenced NSC (P>0.05). Conclusions PPARγ plays roles in the AGE-mediated regulation of NSC proliferation but not neural differentiation through the BDNF-CREB pathway
夏文清、叶宽萍、李凤飞、周祎、王少华、黄艳
基础医学神经病学、精神病学分子生物学
糖基化终产物PPARγ神经干细胞神经再生BDNF-CREB通路
EndocrinologyAdvanced glycation end productsPPARγNeural stem cellsNeurogenesisBDNF-CREB pathway
夏文清,叶宽萍,李凤飞,周祎,王少华,黄艳.PPARγ介导AGEs经BDNF-CREB通路调节神经干细胞增殖[EB/OL].(2011-12-12)[2025-08-11].http://www.paper.edu.cn/releasepaper/content/201112-292.点此复制
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