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Comparison of HIF1A-AS1 and HIF1A-AS2 in regulating HIF-1α and the osteogenic differentiation of PDLCs under hypoxia

Hypoxia-inducible factor-1α (HIF-1α) is essential for regulating the osteogenic differentiation of periodontal ligament cells (PDLCs). The regulatory mechanism of HIF-1α transcription is still not clear. Recently, two long non-coding RNAs, HIF1A antisense RNA 1 (HIF1A-AS1) and HIF1A antisense RNA 2...

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Published in:International journal of molecular medicine 2017-11, Vol.40 (5), p.1529-1536
Main Authors: Chen, Dongru, Wu, Liping, Liu, Lu, Gong, Qimei, Zheng, Jinxuan, Peng, Caixia, Deng, Jianqing
Format: Article
Language:English
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Summary:Hypoxia-inducible factor-1α (HIF-1α) is essential for regulating the osteogenic differentiation of periodontal ligament cells (PDLCs). The regulatory mechanism of HIF-1α transcription is still not clear. Recently, two long non-coding RNAs, HIF1A antisense RNA 1 (HIF1A-AS1) and HIF1A antisense RNA 2 (HIF1A-AS2), were found to regulate HIF-1α mRNA, but the regulatory mechanisms among HIF-1α, HIF1A-AS1 and HIF1A-AS2 have not been well studied. We hypothesized that HIF1A-AS1 and HIF1A-AS2 play important roles in the osteogenic differentiation of PDLCs by regulating HIF-1α. In the present study, we showed that expression levels of HIF1A-AS1, HIF1A-AS2, HIF-1α and osteogenic biomarkers were time-dependent under hypoxia. Even though both HIF1A-AS1 and HIF1A-AS2 were complementary to HIF-1α mRNA, only HIF1A-AS2 showed an inhibitory effect on HIF-1α in PDLCs. Moreover, HIF-1α had positive regulatory effects on HIF1A-AS1 and HIF1A-AS2. HIF-1α promoted the osteogenic differentiation of PDLCs, and HIF1A-AS2 had a negative effect on the osteogenic differentiation of PDLCs. Altogether, the present study revealed the complex relationships among HIF1A-AS1, HIF1A-AS2 and HIF-1α, as well as their roles in regulating the osteogenic differentiation of PDLCs. These findings provide a theoretical basis for promoting periodontal tissue regeneration and repair during orthodontic tooth movement.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2017.3138