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首页> 外文期刊>Life sciences >Pigment epithelium-derived factor inhibits advanced glycation end-product-induced angiogenesis and stimulates apoptosis in retinal endothelial cells.
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Pigment epithelium-derived factor inhibits advanced glycation end-product-induced angiogenesis and stimulates apoptosis in retinal endothelial cells.

机译：色素上皮衍生因子抑制晚期糖基化终产物诱导的血管生成，并刺激视网膜内皮细胞凋亡。

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AIMS: The purpose of this study was to investigate the effect of pigment epithelium-derived factor (PEDF) on the signaling cascade in porcine retinal endothelial cells (PRECs) related to angiogenesis induced by advanced glycation end-products (AGEs). MAIN METHODS: Endothelial cells were isolated from porcine retina by the enzymatic method. Immunocytochemistry was performed to confirm the identity of PRECs. The effect of AGEs and PEDF on cell viability was determined by the MTT assay. An in vitro wound-scratch assay was performed to study the migration of ECs, and in vitro tube formation was assessed by the on-gel assay system using an extracellular matrix. Inhibitor assays were carried out using LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, and Akt inhibitor VIII. PI3K/Akt activity was assessed by transient transfection and western blot analysis. Induction of apoptosis by PEDF was determined by caspase-3 colorimetric assay and DNA fragmentation analysis. KEY FINDINGS: Treatment of PRECs with AGE-bovine serum albumin (AGE-BSA) significantly increased the cell proliferation, migration and tube formation compared to non-glycated BSA. AGE-BSA mediates cell survival via the PI3K/Akt/FKHR-dependent pathway as evidenced by transient transfection and western blot analyses. Furthermore, PEDF significantly inhibited the proliferation, migration and tube formation, both in the presence and absence of AGE-BSA in PRECs. PEDF inactivated the AGE-BSA-induced PI3K/Akt/FKHR activity and induced apoptosis via caspase-3. SIGNIFICANCE: The results reveal that PEDF inhibits AGE-BSA-induced PI3K/Akt/FKHR signaling in PRECs. Thus, PEDF has potent anti-angiogenic effects against AGE-induced angiogenesis and is suggested to be a promising molecule for the treatment of diabetic retinopathy.
机译：目的：本研究的目的是研究色素上皮衍生因子（PEDF）对猪视网膜内皮细胞（PRECs）信号级联反应的影响，该信号通路与晚期糖基化终产物（AGEs）诱导的血管生成有关。主要方法：采用酶法从猪视网膜中分离内皮细胞。进行了免疫细胞化学检查以确认PRECs的身份。通过MTT测定确定AGEs和PEDF对细胞活力的影响。进行了体外划伤试验以研究EC的迁移，并通过使用细胞外基质的凝胶上试验系统评估了体外试管的形成。使用LY294002，磷脂酰肌醇3-激酶（PI3K）抑制剂和Akt抑制剂VIII进行抑制剂测定。通过瞬时转染和蛋白质印迹分析评估PI3K / Akt活性。通过caspase-3比色测定和DNA片段分析确定PEDF诱导的凋亡。关键发现：与非糖化BSA相比，用AGE-牛血清白蛋白（AGE-BSA）处理PRECs显着提高了细胞增殖，迁移和管形成。 AGE-BSA通过PI3K / Akt / FKHR依赖性途径介导细胞存活，瞬时转染和Western blot分析证明了这一点。此外，在PRECs中存在和不存在AGE-BSA的情况下，PEDF均显着抑制增殖，迁移和管形成。 PEDF使AGE-BSA诱导的PI3K / Akt / FKHR活性失活，并通过caspase-3诱导凋亡。意义：结果表明，PEDF抑制PRECs中AGE-BSA诱导的PI3K / Akt / FKHR信号传导。因此，PEDF对AGE诱导的血管生成具有有效的抗血管生成作用，被认为是治疗糖尿病性视网膜病的有前途的分子。

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