Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes.
Ionic silicon improves endothelial cells' survival under toxic oxidative stress by overexpressing angiogenic markers and antioxidant enzymes.
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离子硅通过过表达血管生成标记和抗氧化剂酶在毒性氧化应激下改善内皮细胞的存活。
DOI：
10.1002/term.2744
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发表时间：
2018-11
影响因子：
3.3
通讯作者：
Varanasi VG
中科院分区：
文献类型：
--
作者：
Monte F;Cebe T;Ripperger D;Ighani F;Kojouharov HV;Chen BM;Kim HKW;Aswath PB;Varanasi VG
由有害水平的活性氧引起的氧化应激是一种常见的现象，其通过损害内皮细胞功能而损害适当的骨缺损血管愈合。硅基生物材料释放的硅离子可上调缺氧诱导因子-1 α（HIF-1α）。然而，尚不清楚离子硅是否可以恢复氧化应激条件下的内皮细胞功能。因此，我们假设离子硅可以帮助改善人脐静脉内皮细胞（HUVECs）在毒性氧化应激下的存活。在这项研究中，我们评估了在正常条件下和有害的过氧化氢水平下，离子硅对HUVECs活力、增殖、迁移、基因表达和毛细血管形成的影响。我们证明，在正常条件下，0.5-mM Si 4+显著增强HUVEC中的血管生成（p < 0.05）。暴露于0.5-mM Si 4+的HUVEC呈现出形态学变化，即使没有基质胶床，并且形成比对照显著更多的管状结构（p < 0.001）。此外，0.5 mM Si 4+增强了有害H2 O2水平下HUVEC的细胞活力。在正常和毒性H2 O2条件下，硅处理的HUVECs中HIF-1α、血管内皮生长因子-A和血管内皮生长因子受体-2过表达超过两倍。此外，在正常和氧化应激环境下，用0.5-mM Si 4+过表达的超氧化物歧化酶-1（SOD-1）、过氧化氢酶-1（Cat-1）和一氧化氮合酶-3（NOS 3）处理HUVEC（p < 0.01）。计算模型用于解释Si 4+在内皮细胞和人骨膜细胞中通过SOD-1增强的抗氧化作用。总之，我们证明了0.5 mM Si 4+可以通过减少细胞死亡和上调血管生成因子和抗氧化因子的表达来恢复氧化应激条件下的HUVEC活力。
Oxidative stress, induced by harmful levels of reactive oxygen species, is a common occurrence that impairs proper bone defect vascular healing through the impairment of endothelial cell function. Ionic silicon released from silica-based biomaterials, can upregulate hypoxia-inducible factor-1α (HIF-1α). Yet it is unclear whether ionic Si can restore endothelial cell function under oxidative stress conditions. Therefore, we hypothesized that ionic silicon can help improve human umbilical vein endothelial cells’ (HUVECs’) survival under toxic oxidative stress. In this study, we evaluated the ionic jsilicon effect on HUVECs viability, proliferation, migration, gene expression, and capillary tube formation under normal conditions and under harmful hydrogen peroxide levels. We demonstrated that 0.5-mM Si4+ significantly enhanced angiogenesis in HUVECs under normal condition (p < 0.05). HUVECs exposed to 0.5-mM Si4+ presented a morphological change, even without the bed of Matrigel, and formed significantly more tube-like structures than the control (p < 0.001). In addition, 0.5-mM Si4+ enhanced cell viability in HUVECs under harmful H2O2 levels. HIF-1α, vascular endothelial growth factor-A, and vascular endothelial growth factor receptor-2 were overexpressed more than twofold in silicon-treated HUVECs, under normal and toxic H2O2 conditions. Moreover, the HUVECs were treated with 0.5-mM Si4+ overexpressed superoxide dismutase-1 (SOD-1), catalase-1 (Cat-1), and nitric oxide synthase-3 (NOS3) under normal and oxidative stress environment (p < 0.01). A computational model was used for explaining the antioxidant effect of Si4+ in endothelial cells and human periosteum cells by SOD-1 enhancement. In conclusion, we demonstrated that 0.5-mM Si4+ can recover the HUVECs’ viability under oxidative stress conditions by reducing cell death and upregulating expression of angiogenic and antioxidant factors.
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影响因子：
8.6
作者：
KARDAR, M;PARISI, G;ZHANG, YC
通讯作者：
ZHANG, YC
影响因子：
82.9
作者：
Aicher, A;Heeschen, C;Dimmeler, S
通讯作者：
Dimmeler, S
影响因子：
10
作者：
Ilyas A;Odatsu T;Shah A;Monte F;Kim HK;Kramer P;Aswath PB;Varanasi VG
通讯作者：
Varanasi VG
影响因子：
2.1
作者：
Davis, George E.;Koh, Wonshill;Stratman, Amber N.
通讯作者：
Stratman, Amber N.
影响因子：
20.1
作者：
Galasso, G;Schiekofer, S;Walsh, K
通讯作者：
Walsh, K