Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6280871 | Neuroscience Letters | 2015 | 6 Pages |
Abstract
Circadian rhythm disorder is a common neurological deficit caused by neonatal hypoxic-ischemic brain damage (HIBD). However, little is known about its underlying mechanisms. Our previous studies revealed a significant elevation of clock genes at the protein, but not mRNA, levels in the pineal gland after neonatal HIBD. To investigate the mechanisms of post-transcriptional regulation on clock genes, we screened changes of miRNA levels in the pineal gland after neonatal HIBD using high-throughput arrays. Within the miRNAs whose expression was significantly down-regulated, we identified one miRNA (miR182) that targeted the 3â²-untranslated region (3â²-UTR) of Clock, a key component of clock genes, and played a crucial role in regulating CLOCK expression after oxygen-glucose deprivation in primarily cultured pinealocytes. Our findings therefore provide new insight on studies of therapeutic targets for circadian rhythm disturbance after neonatal HIBD.
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Authors
Xin Ding, Bin Sun, Jian Huang, Lixiao Xu, Jian Pan, Chen Fang, Yanfang Tao, Shukun Hu, Ronghu Li, Xing Han, Po Miao, Ying Wang, Jian Yu, Xing Feng,