Protective effects of lncRNA H19 silence against hypoxia-induced injury in PC-12 cells by regulating miR-28

LncRNA H19 has been widely reported to be up-regulated upon hypoxia. We aimed to uncover the function and mechanism of IncRNA H19 in hypoxic PC-12 cells. Neural-like PC-12 cells were exposed to hypoxia to stimulating an in vitro model of hypoxic brain damage. The expression levels of IncRNA H19 in PC-12 cells were altered by transfection, then cell viability, migration and apoptosis were assessed respectively. Moreover, the cross regulation between IncRNA H19, miR-28 and SP1 was studied to reveal one of the possible mechanisms of IncRNA H19's function. We found that hypoxia induced remarkable decreases in cell viability and migration, and induced a notable increase in cell apoptosis. Hypoxia-induced cell damage was aggravated by IncRNA H19 overexpression, while was alleviated by IncRNA H19 silence. miR-28 was negatively regulated by lncRNA H19, and SP1 was a target gene of miR-28. Furthermore, IncRNA H19 down-regulated miR-28 expression, which in turn preventing SP1 from degradation by miR-28, and ultimately deactivated PDK/AKT and JAK/STAT signaling pathways. In conclusion, our research demonstrated a protective role of IncRNA H19 silence in hypoxic PC-12 cells. A possible mechanism of which IncRNA H19 functioned to PC-12 cells was that IncRNA H19 down regulated miR-28 expression, preventing SP1 exhausted by miR-28. (C) 2018 Elsevier B.V. All rights reserved.