Promotional effects of HIF1α and KDM3A interaction on vascular smooth muscle cells in thoracic aortic dissection.

Aim: The current study was performed to define the role of KDM3A in thoracic aortic dissection (TAD).

Methods

The binding of HIF1α and KDM3A in HES1 was detected by ChIP and dual-luciferase reporter gene assay. Loss and gain-of function assays of HIF1α, KDM3A and HES1 were further performed in Ang-II-induced mouse aortic smooth muscle cell line (MOVAS) cells. Lastly, in vivo TAD models were established.

Results

HIF1α was highly expressed in TAD. KDM3A promoted the transcription activation of HES1. HIF1α enhanced the proliferation and migration of Ang-II-induced MOVAS cells, in addition to increasing thoracic aorta dilation to induce TAD formation in vivo. Silencing of HES1 reversed the effects of HIF1α in vivo and in vitro.

Conclusion

The findings indicated that interaction between HIF1α and KDM3A enhances the proliferation and migration of MOVAS cells to induce TAD.