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Author Sun, Xingyuan ♦ Ren, Zhanjun ♦ Pan, Yunzhi ♦ Zhang, Chenxin
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANIMAL TISSUES ♦ ANOXIA ♦ APOPTOSIS ♦ BRAIN ♦ CELL CYCLE ♦ CELL PROLIFERATION ♦ INJURIES ♦ ISCHEMIA ♦ LUCIFERASE ♦ MESSENGER-RNA ♦ NERVE CELLS ♦ PATIENTS
Abstract Hypoxia-induced apoptosis-related mechanisms involved in the brain damage following cerebral ischemia injury. A subset of the small noncoding microRNA (miRNAs) is regulated by tissue oxygen levels, and miR-24 was found to be activated by hypoxic conditions. However, the roles of miR-24 and its target gene in neuron are not well understood. Here, we validated miRNA-24 is down-regulated in patients with cerebral infarction. Hypoxia suppressed the expression of miR-24, but increased the expression of neurocan in both mRNA and protein levels in SH-SY5Y cells. MiR-24 mimics reduced the expression of neurocan, suppressed cell apoptosis, induced cell cycle progression and cell proliferation in SH-SY5Y cells under hypoxia. By luciferase reporter assay, neurocan is validated a direct target gene of miR-24. Furthermore, knockdown of neurocan suppressed cell apoptosis, induced cell cycle progression and cell proliferation in SH-SY5Y cells under hypoxia. Taken together, miR-24 overexpression or silencing of neurocan shows an antihypoxic effect in SH-SY5Y cells. Therefore, miR-24 and neurocan play critical roles in neuron cell apoptosis and are potential therapeutic targets for ischemic brain disease. - Highlights: • miR-24 and neurocan play critical roles in neuron cell apoptosis. • miR-24 and neurocan are potential therapeutic targets for ischemic brain disease. • Antihypoxic effect of miR-24 and neurocan in SH-SY5Y cells.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2016-09-02
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 477
Issue Number 4


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