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<p>Diabetic retinopathy is a retinal damage, which causes vision impairment and blindness. Integrin Subunit Alpha 5 (ITGA5) regulates angiogenic response, but its roles in diabetic retinopathy remain unclear. In this work, diabetes mellitus was induced in rats by streptozotocin. ITGA5 interference was achieved by intravitreal delivery of adeno-associated virus. Upregulation of ITGA5 was found in diabetic rat retinal tissues. ITGA5 knockdown decreased the neovascularization, acellular capillary formation, and pericytes. The protein expression of vascular endothelial growth factor (VEGFA), vascular adhesion molecule-1(VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) was reduced after ITGA5 interference. Besides, ITGA5 knockdown decreased the phosphorylation level of FAK, TAK-1, and p65. In vitro, rat retinal microvascular endothelial cells (RRMECs) were cultured under high glucose condition to stimulate diabetic environment. ITGA5 knockdown inhibited VEGFA secretion, tube formation, cell invasion, and migration. Upregulation of VCAM-1 and ICAM-1 that induced by high glucose was reversed by ITGA5 silencing. ITGA5 knockdown blocked the activation of TAK-1/NF-kB pathway in RRMECs. Additionally, in oxygen-induced retinopathy model, ITGA5 interference inhibited pathological neovascularization. These results demonstrate that ITGA5 contributes to the angiogenesis in diabetic retinopathy by activating TAK-1/NF-kB pathway.</p>

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ITGA5 drives angiogenesis in diabetic retinopathy via TAK-1/NF-kB activation

  • 期刊论文

  • 发表日期：

    2025年5月23日

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  • Feifei Kan,
  • Di Wang,
  • Sijia Li,
  • Yi Gao,
  • Jianwen Wang

摘要

Diabetic retinopathy is a retinal damage, which causes vision impairment and blindness. Integrin Subunit Alpha 5 (ITGA5) regulates angiogenic response, but its roles in diabetic retinopathy remain unclear. In this work, diabetes mellitus was induced in rats by streptozotocin. ITGA5 interference was achieved by intravitreal delivery of adeno-associated virus. Upregulation of ITGA5 was found in diabetic rat retinal tissues. ITGA5 knockdown decreased the neovascularization, acellular capillary formation, and pericytes. The protein expression of vascular endothelial growth factor (VEGFA), vascular adhesion molecule-1(VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) was reduced after ITGA5 interference. Besides, ITGA5 knockdown decreased the phosphorylation level of FAK, TAK-1, and p65. In vitro, rat retinal microvascular endothelial cells (RRMECs) were cultured under high glucose condition to stimulate diabetic environment. ITGA5 knockdown inhibited VEGFA secretion, tube formation, cell invasion, and migration. Upregulation of VCAM-1 and ICAM-1 that induced by high glucose was reversed by ITGA5 silencing. ITGA5 knockdown blocked the activation of TAK-1/NF-kB pathway in RRMECs. Additionally, in oxygen-induced retinopathy model, ITGA5 interference inhibited pathological neovascularization. These results demonstrate that ITGA5 contributes to the angiogenesis in diabetic retinopathy by activating TAK-1/NF-kB pathway.