Inhibition of EZH2 suppresses peritoneal angiogenesis by targeting a VEGFR2/ERK1/2/HIF-1α-dependent signaling pathway.
Yingfeng ShiJinqing LiHui ChenYan HuLunxian TangYi WangXiujuan ZangXiaoyan MaGuansen HuangXun ZhouMin TaoZexin LvSi ChenAndong QiuShougang ZhuangNa LiuPublished in: The Journal of pathology (2022)
The catalytic subunit of polycomb repressive complex 2 (PRC2), enhancer of zeste homolog 2 (EZH2), has been reported to be involved in angiogenesis in some tumors and autoimmune diseases. However, the mechanisms by which EZH2 regulates peritoneal angiogenesis remain unclear. We detected the expression of EZH2 in clinical samples and the peritoneal tissue of a mouse peritoneal fibrosis model induced by chlorhexidine gluconate (CG). In addition, we further investigated the mechanisms by which inhibition of EZH2 by 3-deazaneplanocin A (3-DZNeP) alleviated the CG-induced peritoneal fibrosis mouse model in vivo and 3-DZNeP or EZH2 siRNA treatment in cultured human peritoneal mesothelial cells (HPMCs) and human umbilical vein endothelial cells (HUVECs). The expression of EZH2 in the peritoneum of long-term peritoneal dialysis (PD) patients and the CG-induced peritoneal fibrosis mouse model was remarkably increased and this was positively associated with higher expression of vascular markers (CD31, CD34, VEGF, p-VEGFR2). Peritoneal injection of 3-DZNeP attenuated angiogenesis in the peritoneum of CG-injured mice; improved peritoneal membrane function; and decreased phosphorylation of STAT3, ERK1/2, and activation of Wnt1/β-catenin. In in vitro experiments, we demonstrated that inhibition of EZH2 by 3-DZNeP or EZH2 siRNA decreased tube formation and the migratory ability of HUVECs via two pathways: the Wnt1/β-catenin pathway and the IL-6/STAT3 pathway. Suppression of the Wnt1/β-catenin pathway and the IL-6/STAT3 pathway subsequently reduced VEGF production in HPMCs. Using specific inhibitors of VEGFR2, ERK1/2, and HIF-1α, we found that a VEGFR2/ERK1/2/HIF-1α axis existed and contributed to angiogenesis in vitro. Moreover, phosphorylation of VEGFR2 and activation of the ERK1/2 pathway and HIF-1α in HUVECs could be suppressed by inhibition of EZH2. Taken together, the results of this study suggest that EZH2 may be a novel target for preventing peritoneal angiogenesis in PD patients. © 2022 The Pathological Society of Great Britain and Ireland.
Keyphrases
- endothelial cells
- high glucose
- vascular endothelial growth factor
- signaling pathway
- cell proliferation
- end stage renal disease
- long non coding rna
- long noncoding rna
- peritoneal dialysis
- poor prognosis
- pi k akt
- mouse model
- chronic kidney disease
- induced apoptosis
- stem cells
- newly diagnosed
- epithelial mesenchymal transition
- binding protein
- ejection fraction
- type diabetes
- cell cycle arrest
- wound healing
- endoplasmic reticulum stress
- oxidative stress
- cancer therapy
- transcription factor
- patient reported
- diabetic rats
- protein kinase
- metabolic syndrome
- high speed