Angiogenic ability of human endothelial cells was decreased following senescence induction with hydrogen peroxide: possible role of vegfr-2/akt-1 signaling pathway.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2022-07-25 DOI:10.1186/s12860-022-00435-4

Nesa Janamo Berenjabad, Vahid Nejati, Jafar Rezaie

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引用次数: 3

Abstract

Background: Many attempts are used to discover mechanisms driving impaired angiogenesis in age-related diseases. Angiogenesis is highly regulated by different signaling pathways. Here, we investigated the angiogenesis potential of human endothelial cells (ECs) upon exposure to hydrogen peroxide (H₂O₂), a cellular senescent factor.

Results: Data showed that the wound healing rate of HUVECs decreased upon incubation with H₂O₂ (P < 0.05). LOX activity and NO production were decreased in H₂O₂ treated cells (P < 0.05). Expression of miR-126 and VEGFR-2 up-regulated, while expression of miR-373 and HSP-70 up = regulated in H₂O₂ -induced cells (P < 0.05). In addition, we found that protein levels of p-Akt-1, VCAM-1, MMP-9, and IL-6 decreased in treated cells (P < 0.05).

Conclusions: Our data showed that H₂O₂ reduced the angiogenic response of HUVECs in vitro, which may be due to impairment of the VEGFR-2 signaling pathway.

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过氧化氢诱导衰老后，人内皮细胞的血管生成能力下降:可能与vegfr-2/akt-1信号通路有关。

背景:许多研究试图发现衰老相关疾病中血管生成受损的机制。血管生成受不同信号通路的高度调控。在这里，我们研究了暴露于过氧化氢(H2O2)(一种细胞衰老因子)后人内皮细胞(ECs)的血管生成潜力。结果:数据显示H2O2 (p2o2)处理细胞(p2o2)诱导的HUVECs伤口愈合速率降低。结论:我们的数据显示H2O2降低了HUVECs体外血管生成反应，这可能与VEGFR-2信号通路受损有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464