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首页> 外文期刊>The international journal of biochemistry and cell biology >Thioredoxin-interacting protein deficiency ameliorates diabetic retinal angiogenesis
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Thioredoxin-interacting protein deficiency ameliorates diabetic retinal angiogenesis

机译：患有毒素相互作用的蛋白质缺乏改善糖尿病视网膜血管生成

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Abstract Diabetic retinopathy is the leading cause of blindness among working-aged adults around the world. Hyperglycemia and intraocular vascular endothelial growth factor (VEGF) over-accumulation are essential for the progression of diabetic retinopathy, which eventually results in proliferative diabetic retinopathy, characterized by pathologic angiogenesis and impaired vision. Thioredoxin-interacting protein (TXNIP) was highly induced in retinal endothelial cells under diabetic conditions. However, the role of TXNIP in diabetes-associated retinal angiogenesis remains elusive. Here, we investigated whether the absence of TXNIP alters diabetes-associated retinal angiogenesis. Exposure of human retinal microvascular endothelial cells (HRMECs) to moderately high glucose (MHG) promoted cell migration and tube formation, but not proliferation. Knockdown of TXNIP suppressed moderately high glucose (MHG)-induced reactive oxygen species (ROS) generation, migration, tube formation and activation of Akt/mTOR pathway in HRMECs. Moreover, gene silencing of TXNIP inhibited VEGF-induced angiogenic response by blocking VEGFR2 and downstream signal pathway Akt/mTOR activation in HRMECs. Furthermore, TXNIP knockout inhibited VEGF or VEGF and MHG-induced retinal angiogenesis ex vivo compared with wild-type mice. In conclusion, our study demonstrated that TXNIP deficiency inhibited VEGF or/and MHG-induced angiogenic response in HRMECs and mice retinas and suggested TXNIP may be a potential therapy target for treating proliferative diabetic retinopathy.
机译：摘要糖尿病视网膜病变是世界各地工作老年人失明的主要原因。高血糖和眼内血管内皮生长因子（VEGF）过度积累对于糖尿病视网膜病变的进展至关重要，最终导致增殖性糖尿病视网膜病变，其特征在于病理血管生成和视力受损。在糖尿病条件下，患有硫昔林 - 相互作用的蛋白（TXNIP）高度诱导视网膜内皮细胞。然而，TXNIP在糖尿病相关视网膜血管生成的作用仍然难以捉摸。在这里，我们研究了是否存在TXNIP改变糖尿病相关的视网膜血管生成。将人视网膜微血管内皮细胞（HRMECs）暴露于中度高葡萄糖（MHG）促进细胞迁移和管形成，但不能增殖。 TXNIP的敲低抑制了中度高葡萄糖（MHG）诱导的活性氧（ROS）产生，迁移，管形成和HRMEC中Akt / mTOR途径的活化。此外，TXNIP的基因沉默通过阻断HRMEC中的VEGFR2和下游信号通路Akt / mTOR活化来抑制VEGF诱导的血管生成响应。此外，与野生型小鼠相比，TXNIP敲除抑制VEGF或VEGF和MHG诱导的视网膜血管生成。总之，我们的研究表明，TXNIP缺乏抑制HRMECs和小鼠视网膜中的VEGF或/和MHG诱导的血管生成反应，并且建议的TXNIP可以是治疗增殖性糖尿病视网膜病变的潜在治疗靶标。

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