Promotional effects of HIF1α and KDM3A interaction on vascular smooth muscle cells in thoracic aortic dissection.
Zheyong LiangQi LiangWei ZhangLei ZhengXuji ShenYongjian ZhangPublished in: Epigenomics (2022)
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.
Keyphrases
- aortic dissection
- induced apoptosis
- endothelial cells
- cell cycle arrest
- smooth muscle
- vascular smooth muscle cells
- angiotensin ii
- high glucose
- spinal cord
- high throughput
- aortic valve
- oxidative stress
- pulmonary artery
- cell death
- gene expression
- left ventricular
- spinal cord injury
- dna methylation
- coronary artery
- copy number
- drug induced