MicroRNA-210 Protects PC-12 Cells Against Hypoxia-Induced Injury by Targeting BNIP3
| Autor: | Yubin Dong, Xiaoli Zhang, Yonggang Luan, Yongli Zhang |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
neonatal brain injury BNIP3 Kinase PI3K/AKT/mTOR signal pathway microRNA-210 RPTOR Transfection Biology lcsh:RC321-571 Cell biology 03 medical and health sciences Cellular and Molecular Neuroscience 030104 developmental biology Apoptosis microRNA Viability assay lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry hypoxic injury Protein kinase B PI3K/AKT/mTOR pathway Neuroscience Original Research |
| Zdroj: | Frontiers in Cellular Neuroscience Frontiers in Cellular Neuroscience, Vol 11 (2017) |
| ISSN: | 1662-5102 |
| DOI: | 10.3389/fncel.2017.00285 |
| Popis: | MicroRNA (miR)-210 is the most consistently and predominantly up-regulated miR in response to hypoxia in multiple cancer cells. The roles of miR-210 in rat adrenal gland pheochromocytoma (PC-12) cells remain unknown. We aimed to explore the possible effect of miR-210 in neonatal brain injury. We explored the potential molecular mechanism by using PC-12 cells under hypoxia. Scramble miRs, miR-210 mimic, miR-210 inhibitor or its negative control were respectively transfected into PC-12 cells. Cell viability, migration, invasion and apoptosis were also assessed to evaluate hypoxia-induced cell injury. The expression level of miR-210 was identified by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Apoptosis-related protein expression as well as key kinases in the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signal pathway was studied by Western blot analysis. Hypoxia suppressed cell viability, migration and invasion, but promoted apoptosis through activation of mitochondrial- and caspase-dependent pathways. Hypoxia markedly induced up-regulation of miR-210 in PC-12 cells. Overexpression of miR-210 protected PC-12 cells against hypoxia-induced injury. Bcl-2 adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) was proven to be a target gene of miR-210 in PC-12 cells. miR-210 overexpression ameliorated the hypoxia-induced injury in PC-12 cells by down-regulating BNIP3. Hypoxia-induced alterations of key kinases in the PI3K/AKT/mTOR signal pathway were affected by aberrant expression of BNIP3. These findings suggested that miR-210 protected PC-12 cells against hypoxia-induced injury by targeting BNIP3, involving the PI3K/AKT/mTOR signal pathway. |
| Databáze: | OpenAIRE |
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