Mitochondrial uncoupling protein 2 is regulated through heterogeneous nuclear ribonucleoprotein K in lead exposure models
Mitochondrial uncoupling protein 2 is regulated through heterogeneous nuclear ribonucleoprotein K in lead exposure models
复制标题
在铅暴露模型中，线粒体解偶联蛋白 2 通过异质核核糖核蛋白 K 进行调节
DOI：
10.1080/26896583.2020.1854596
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发表时间：
2020
影响因子：
2.5
通讯作者：
Chen Hongping
中科院分区：
文献类型：
--
作者：
Zhu Gaochun;Zhu Qian;Zhang Wei;Hui Chen;Li Yuwen;Yang Meiyuan;Pang Shimin;Li Yaobing;Xue Guoyong;Chen Hongping
突触可塑性在海马发育过程中的学习记忆中起着重要作用。然而，在铅暴露模型中精确的分子机制仍有待研究。UCP 2是线粒体内阴离子载体，通过解偶联神经元调节突触可塑性。hnRNP K是一种RNA结合蛋白，在调节编码突触可塑性的转录本的表达中起作用。我们的目的是调查是否铅暴露影响UCP 2和hnRNP K的表达水平。将Sprague-Dawley大鼠在妊娠期和哺乳期暴露于不同浓度的醋酸铅（0 g/l、0.5 g/l、2.0 g/l）。将PC 12细胞暴露于不同浓度的醋酸铅（0 μM、1 μM和100 μM）。结果发现，铅暴露后大鼠海马和PC 12细胞中UCP 2和hnRNP K的表达水平明显下降。在铅暴露模型中，hnRNP K表达水平的上调可逆转UCP 2的表达水平。提示铅暴露可降低UCP 2的表达水平，其机制可能是通过降低hnRNP K的表达水平而实现的。
Synaptic plasticity plays an important role in learning and memory in the developing hippocampus. However, the precise molecular mechanism in lead exposure models remains to be studied. UCP2, an inner mitochondrial anion carrier, regulates synaptic plasticity through uncoupling neurons. And hnRNP K, an RNA binding protein, plays a role in modulating the expression of transcripts coding synaptic plasticity. We aim to investigate whether lead exposure affects UCP2 and hnRNP K expression levels. The Sprague-Dawley rats were exposed to different lead acetate concentrations (0 g/l, 0.5 g/l, 2.0 g/l) during gestational and lactational periods. PC12 cells were also exposed to different lead acetate concentrations (0 μM, 1 μM and 100 μM). We found that the expression levels of UCP2 and hnRNP K had significant declines in the lead exposure rat hippocampus and PC12 cells. Furthermore, the up-regulation of hnRNP K expression level could reverse the expression level of UCP2 in lead exposure models. In conclusion, these results suggest that lead exposure can reduce the expression level of UCP2 which is mediated by decreasing the expression level of hnRNP K.