The Effects of Intelectin-1 on Antioxidant and Angiogenesis in HUVECs Exposed to Oxygen Glucose Deprivation

• Published in: Frontiers in neurology Vol. 10; p. 383
• Main Authors: Gu, Naibing, Wang, Jun, Di, Zhengli, Liu, Zhiqin, Jia, Xiaotao, Yan, Yu'e, Chen, Xiaoshan, Zhang, Quanzeng, Qian, Yihua
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 16.04.2019
• Subjects: angiogenesis; apoptosis; HUVECs; intelectin-1; Neurology; OGD; oxidative stress; angiogenesis; apoptosis; intelectin-1; OGD; HUVECs; oxidative stress; PI3K/Akt
• ISSN: 1664-2295; 1664-2295
• DOI: 10.3389/fneur.2019.00383

Ischemic stroke leads to cellular death and tissue damage by depriving the areas of glucose and oxygen supplies. The effective treatment of stroke remains a challenge for modern medicine. This study used an oxygen-glucose deprivation (OGD) model of human umbilical vein endothelial cells (HUVECs) to mimic ischemic injuries and explored the role and mechanism of intelectin-1. Intelectin-1 was transduced into the HUVECs using a lentiviral vector. The PI3K/Akt signaling was examined in intelectin-induced eNOS phosphorylation. The PI3K inhibitor LY294002 was dealed in HUVECs. Our results demonstrated an increase in capillary density, decrease in apoptotic cells, and increase in HIF-1α protein expression following intelectin-1 treatment. Real-time PCR and Western blotting revealed the increased intelectin-1 expression alongside eNOS and Akt phosphorylation with enhanced bcl-2 expression under OGD. Capillary density decreased significantly after LY294002 treatment. These results suggest intelectin-1 promotes angiogenesis, inhibits oxidative stress and reduces apoptosis by stimulating the Akt-eNOS signaling pathway in response to ischemia .