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人内皮细胞的血管生成能力在过氧化氢诱导衰老后降低：vegfr-2/akt-1 信号通路的可能作用。

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

机构信息

Department of Biology, Urmia University, Urmia, Iran.

Solid Tumor Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Shafa St, Ershad Blvd, P.O. BoX: 1138, Urmia, Postal Code: 57147, Iran.

出版信息

BMC Mol Cell Biol. 2022 Jul 25;23(1):31. doi: 10.1186/s12860-022-00435-4.

DOI:10.1186/s12860-022-00435-4
PMID:35879650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9310472/
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 (HO), a cellular senescent factor.

RESULTS

Data showed that the wound healing rate of HUVECs decreased upon incubation with HO (P < 0.05). LOX activity and NO production were decreased in HO 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 HO -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 HO reduced the angiogenic response of HUVECs in vitro, which may be due to impairment of the VEGFR-2 signaling pathway.

摘要

背景

许多研究都试图探索导致与年龄相关的疾病中血管生成受损的机制。血管生成受到不同信号通路的高度调节。在这里，我们研究了人内皮细胞（EC）在暴露于过氧化氢（HO）时的血管生成潜力，HO 是一种细胞衰老因子。

结果

数据显示，孵育 HO 后 HUVEC 的伤口愈合率降低（P<0.05）。HO 处理的细胞中 LOX 活性和 NO 产生减少（P<0.05）。HO 诱导的细胞中 miR-126 和 VEGFR-2 的表达上调，而 miR-373 和 HSP-70 的表达上调（P<0.05）。此外，我们发现处理细胞中 p-Akt-1、VCAM-1、MMP-9 和 IL-6 的蛋白水平降低（P<0.05）。

结论

我们的数据表明，HO 降低了 HUVECs 的体外血管生成反应，这可能是由于 VEGFR-2 信号通路受损所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/311701bc8847/12860_2022_435_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/e6bf1f283edb/12860_2022_435_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/d3330ea90189/12860_2022_435_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/35a2b140f7e3/12860_2022_435_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/311701bc8847/12860_2022_435_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/e6bf1f283edb/12860_2022_435_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/d3330ea90189/12860_2022_435_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/35a2b140f7e3/12860_2022_435_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59ea/9310472/311701bc8847/12860_2022_435_Fig4_HTML.jpg

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