6'-Sialylgalactose inhibits vascular endothelial growth factor receptor 2-mediated angiogenesis.
Tae-Wook ChungEun-Yeong KimHee-Jung ChoiChang Woo HanSe Bok JangKeuk-Jun KimLing JinYoung Jun KohKi-Tae HaPublished in: Experimental & molecular medicine (2019)
Angiogenesis should be precisely regulated because disordered neovascularization is involved in the aggravation of multiple diseases. The vascular endothelial growth factor (VEGF)-A/VEGF receptor 2 (VEGFR-2) axis is crucial for controlling angiogenic responses in vascular endothelial cells (ECs). Therefore, inactivating VEGFR-2 signaling may effectively suppress aberrant angiogenesis and alleviate related symptoms. In this study, we performed virtual screening, identified the synthetic disaccharide 6'-sialylgalactose (6SG) as a potent VEGFR-2-binding compound and verified its high binding affinity by Biacore assay. 6SG effectively suppressed VEGF-A-induced VEGFR-2 phosphorylation and subsequent in vitro angiogenesis in HUVECs without inducing cytotoxicity. 6SG also inhibited VEGF-A-induced extracellular-regulated kinase (ERK)/Akt activation and actin stress fiber formation in HUVECs. We demonstrated that 6SG inhibited retinal angiogenesis in a mouse model of retinopathy of prematurity and tumor angiogenesis in a xenograft mouse model. Our results suggest a potential therapeutic benefit of 6SG in inhibiting angiogenesis in proangiogenic diseases, such as retinopathy and cancer.
Keyphrases
- vascular endothelial growth factor
- endothelial cells
- high glucose
- mouse model
- signaling pathway
- diabetic rats
- squamous cell carcinoma
- oxidative stress
- transcription factor
- optical coherence tomography
- high throughput
- protein kinase
- young adults
- papillary thyroid
- physical activity
- sleep quality
- dna binding
- lymph node metastasis